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58 gesichtete, geschützte Fragmente: Plagiat

[1.] Haw/Fragment 018 01 - Diskussion
Bearbeitet: 23. October 2014, 19:53 WiseWoman
Erstellt: 13. October 2014, 22:38 (Hindemith)
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Haw 18a diss.png

[84](Dbouk HA, et al., Cell Commun Signal, 2009; 7: 4)

Fig. 1.7. Life cycle and protein associations of connexins. Connexins are synthesized on ER-bound ribosomes and inserted into the ER cotranslationally. This is followed by oligomerization between the ER and trans-Golgi network (depending on the connexin type) into connexons, which are then delivered to the membrane via the actin or microtubule networks. Connexons may also be delivered to the plasma membrane by direct transfer from the rough ER. Upon insertion into the membrane, connexons may remain as hemichannels or they dock with compatible connexons on adjacent cells to form gap junctions[84]. Newly delivered connexons are added to the periphery of pre-formed gap junctions, while the central "older" gap junction fragments are degraded by internalization of a double-membrane structure called an annular junction into one of the two cells, where subsequent lysosomal or proteasomal degradation occurs, or in some cases the connexons are recycled to the membrane (indicated by dashed arrow). During their life cycle, connexins associate with different proteins, including (1) cytoskeletal components as microtubules, actin, and actin-binding proteins α-spectrin and drebrin, (2) junctional molecules including adherens junction components such as cadherins, α-catenin, and β-catenin, as well as tight junction components such as ZO-1 and ZO-2, (3) enzymes such as kinases and phosphatases which regulate the assembly, function, and degradation, and (4) other proteins such as caveolin[84].


84. Dbouk, H.A., et al., Connexins: a myriad of functions extending beyond assembly of gap junction channels. Cell Commun Signal, 2009. 7: p. 4.

Haw 18a source.png

Figure I

Life cycle and protein associations of connexins. Connexins are synthesized on ER-bound ribosomes and inserted into the ER cotranslationally. This is followed by oligomerization between the ER and trans-Golgi network (depending on the connexin type) into connexons, which are then delivered to the membrane via the actin or microtubule networks. Connexons may also be delivered to the plasma membrane by direct transfer from the rough ER. Upon insertion into the membrane, connexons may remain as hemichannels or they dock with compatible connexons on adjacent cells to form gap junctions. Newly delivered connexons are added to the periphery of pre-formed gap junctions, while the central "older" gap junction fragment are degraded by internalization of a double-membrane structure called an annular junction into one of the two cells, where subsequent lysosomal or proteasomal degradation occurs, or in some cases the connexons are recycled to the membrane (indicated by dashed arrow). During their life cycle, connexins associate with different proteins, including (1) cytoskeletal components as microtubules, actin, and actin-binding proteins α-spectrin and drebrin, (2) junctional molecules including adherens junction components such as cadherins, α-catenin, and β-catenin, as well as tight junction components such as ZO-1 and ZO-2, (3) enzymes such as kinases and phosphatases which regulate the assembly, function, and degradation, and (4) other proteins such as caveolin.

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Auf die Quelle wird verwiesen, aber es wird nicht deutlich, dass die gesamte Bildunterschrift wörtlich übernommen ist.

Man beachte auch, dass sich das Bild samt Bildunterschrift auch in der Quelle Wikipedia Connexin (2010) finden läßt. Aus dieser Quelle wurde auf der folgenden Seite Text ungekennzeichnet übernommen.

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(Hindemith), WiseWoman

[2.] Haw/Fragment 021 01 - Diskussion
Bearbeitet: 23. October 2014, 19:49 WiseWoman
Erstellt: 13. October 2014, 21:24 (Hindemith)
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Normal fibre separations in the probe head are a few tenths of 1mm, consequently blood flow is measured in a tissue volume of typically 1mm3 or smaller.

(Fig.1.8.a)

Haw 21a diss.png

(Basic Theory and Operating Principles of LDF & LDI, Moor instruments Ltd User manual, 2003)

In a Laser Doppler blood flow Imager (LDI) the low intensity laser beam is scanned across a tissue surface in a raster fashion using a moving mirror. There is no direct contact with the tissue being assessed. The basic elements of the moorLDI are shown schematically in the following figure.

(Fig.1.8.b)

Haw 21b diss.png

(Basic Theory and Operating Principles of LDF & LDI, Moor instruments Ltd User manual, 2003)

Normal fibre separations in the probe head are a few tenths of a mm, consequently blood flow is measured in a tissue volume of typically 1mm3 or smaller. [...]

(c)

Haw 21a source.png

In a Laser Doppler blood flow Imager (LDI) the low intensity laser beam is scanned across a tissue surface in a raster fashion using a moving mirror. There is no direct contact with the tissue being assessed. The basic elements of the moorLDI are shown schematically in the following figure.

(d)

Haw 21b source.png

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Für die Abbildungen ist die Quelle angegeben, für den Text nicht.

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[3.] Haw/Fragment 014 01 - Diskussion
Bearbeitet: 23. October 2014, 19:44 WiseWoman
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Arteriogenesis differs from angiogenesis in several aspects, (Table 1.1., Fig.1.5.) the most important being the dependence of angiogenesis on hypoxia and the dependence of arteriogenesis on inflammation[20]. However, angiogenesis and arteriogenesis share several mechanisms of action, e.g., their dependence on growth factors. Whereas angiogenesis can be largely explained by the actions of VEGF, arteriogenesis is probably a multifactorial process in which several growth factors are orchestrated. The role of VEGF in arteriogenesis is not clear, but a chemoattractive role for monocytes and hence an indirect contribution is imaginable[21].

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

Arteriogenesis differs from angiogenesis in several aspects, the most important being the

[S. 125]

dependence of angiogenesis on hypoxia and the dependence of arteriogenesis on inflammation.

However, angiogenesis and arteriogenesis share several mechanisms of action (Fig. 2), e.g., their dependence on growth factors. Whereas angiogenesis can be largely explained by the actions of VEGF, arteriogenesis is probably a multifactorial process in which several growth factors are orchestrated. The role of VEGF in arteriogenesis is not clear, but a chemoattractive role for monocytes and hence an indirect contribution is imaginable.

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[4.] Haw/Fragment 013 01 - Diskussion
Bearbeitet: 23. October 2014, 19:33 WiseWoman
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[In another study, Arras, M., et al.[14] injected a single dose of] lipopolysaccharide intravenously into New Zealand white rabbits 3 days after ligation of the femoral artery. This potent stimulator of TNF-a also markedly enhanced the number of monocyte-derived macrophages accumulated around growing collateral arteries. Peripheral and collateral conductance was markedly increased. Nevertheless, on a molar basis MCP-1 is the most potent arteriogenic peptide[21]. VEGF is a peptide with angiogenic properties. It is produced by cells in close vicinity of endothelial cells, its chemoattractive action on monocytes is dose dependent; and its expression is highly regulated by hypoxia and hence by a physiological feedback mechanism to tissue hypoxia[67].

14. Arras, M., et al., Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J Clin Invest, 1998. 101(1): p. 40-50.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

67. Carmeliet, P. and D. Collen, Vascular development and disorders: molecular analysis and pathogenic insights. Kidney Int, 1998. 53(6): p. 1519-49.

In another study, we injected a single dose of lipopolysaccharide intravenously into New Zealand White rabbits 3 days after ligation of the femoral artery (1). This potent stimulator of tumor necrosis factor- a also markedly enhanced the number of monocyte-derived macrophages accumulated around growing collateral arteries. Peripheral and collateral conductances were markedly increased. Nevertheless, on a molar basis MCP-1 is the most potent arteriogenic peptide. Vascular endothelial growth factor (VEGF) is a peptide with angiogenic properties. It is produced by cells in close vicinity of endothelial cells, suggesting paracrine regulation of capillary formation; it is secreted and exerts a direct effect via interaction with endothelial receptors Flk-1 and Flt-1; its chemoattractive action on monocytes is dose dependent; and its expression is highly regulated by hypoxia and thereby a physiological feedback mechanism to tissue hypoxia (3).

1. Arras, M., W. D. Ito, D. Scholz, B. Winkler, J. Schaper, and W. Schaper. Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J. Clin. Invest. 101: 40–50, 1997.

3. Carmeliet, P., and D. Collen. Vascular development and disorders—molecular analysis and pathogenic insights. Kidney Int. 53: 1519–1549, 1998.

Anmerkungen

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[5.] Haw/Fragment 009 20 - Diskussion
Bearbeitet: 23. October 2014, 19:27 WiseWoman
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Upregulation of survival factors for monocytes (granulocyte macrophage colony-stimulating factor (GM-CSF)) provides the environment for a stable function of monocytes (Fig.1.3. C). These in turn produce fairly large amounts of growth factors, including VEGF, colony stimulating factor, transforming growth factor-β, in particular, FGF-2[20]. The adhesion and invasion of monocytes and platelets (also potent producers of growth factors) is soon followed by the first wave of mitosis of the endothelial and smooth muscle cells. The cell invasion is most prominent in the intima, the initial entrance, but even more pronounced later in the adventitia, where they create an inflammatory environment that is later accompanied by T cells. One of the effects of the perivascular inflammation is that it creates the space (by forcing neighboring tissue cells into apoptosis) for the greatly expanding collateral vessel, which can increase its [diameter up to 20 times[21].]

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

Upregulation of survival factors for monocytes (granulocyte macrophage colony-stimulating factor) provides the environment for a stable function of monocytes (Fig. 1C). These in turn produce fairly large amounts of growth factors, in particular, fibroblast growth factor-2. The adhesion and invasion of monocytes and platelets (also potent producers of growth factors) is soon followed by the first wave of mitosis of the endothelial and smooth muscle cells. [...]

[S. 123]

[...] The cell invasion is most prominent in the intima, the initial entrance, but even more pronounced later in the adventitia, where they create an inflammatory environment that is later accompanied by T cells. One of the effects of the perivascular inflammation is that it creates the space (by forcing neighboring tissue cells into apoptosis) for the greatly expanding collateral vessel, which can increase its diameter up to 20 times.

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[6.] Haw/Fragment 013 20 - Diskussion
Bearbeitet: 20. October 2014, 22:11 WiseWoman
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Angiogenesis is a process by which new capillary blood vessels sprout from a pre-existing blood vessel[68]. It is an important component of various normal and pathological conditions such as wound healing, fracture repair, folliculogenesis, ovulation, and pregnancy. These periods of angiogenesis are tightly regulated. However, if not properly controlled, angiogenesis can also represent a significant pathogenic component of tumor growth and metastasis, rheumatic arthritis, and retinopathies[21]. Angiogenesis is a complex phenomenon consisting of several distinct processes, which include endothelial migration and proliferation, extracellular proteolysis, endothelial differentiation (capillary tube formation), and vascular wall remodeling. It is important to recognize that these newly formed capillary tubes lack vascular smooth muscle cells.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

68. Risau, W., Mechanisms of angiogenesis. Nature, 1997. 386(6626): p. 671-4.

Angiogenesis is a process by which new capillary blood vessels sprout from a preexisting blood vessel

[Seite 122]

(10). It is an important component of various normal and pathological conditions such as wound healing, fracture repair, folliculogenesis, ovulation, and pregnancy. These periods of angiogenesis are tightly regulated. However, if not properly controlled, angiogenesis can also represent a significant pathogenic component of tumor growth and metastasis, rheumatic arthritis, and retinopathies. Angiogenesis is a complex phenomenon consisting of several distinct processes, which include endothelial migration and proliferation, extracellular proteolysis, endothelial differentiation (capillary tube formation), and vascular wall remodeling. It is important to recognize that these newly formed capillary tubes lack vascular smooth muscle cells.


10. Risau, W. Mechanisms of angiogenesis. Nature 386: 671–674, 1997.

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[7.] Haw/Fragment 007 07 - Diskussion
Bearbeitet: 20. October 2014, 22:09 WiseWoman
Erstellt: 13. October 2014, 13:24 (Hindemith)
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FSS as a molding force was recognized over 100 years ago; the embryologist Thoma described the relationship between the diameter of an artery and its blood flow velocity[47]. [...] Any sustained deviation from that relationship initiates processes of either growth or atrophy. A sustained increase of fluid shear stress leads to activation of the endothelium.

1.3.3. Activation of the endothelium

It is currently not well enough known how the stimulus of increased shear stress is transmitted from the endothelial cell membrane to the nucleus, where it initiates the transcriptional activity of a number of genes, partially via a protein that binds to the shear stress responsive element that is present in the promotor of several genes (nitric oxide synthase (NOS), platelet-derived growth factor (PDGF), monocyte chemoattractant protein-1 (MCP-1))[49]. The first step in the activation of the endothelium is the opening of chloride channels that are also responsible for the volume control of endothelial cells. Characteristically stress-activated endothelium appears swollen in scanning electron microscopic images[50], adhesion molecules are upregulated[51], and the conditions are perfect for the adhesion and invasion of circulating cells.


47. Yancopoulos, G.D., M. Klagsbrun, and J. Folkman, Vasculogenesis, angiogenesis, and growth factors: ephrins enter the fray at the border. Cell, 1998. 93(5): p. 661-4.

49. Shyy, Y.J., et al., Fluid shear stress induces a biphasic response of human monocyte chemotactic protein 1 gene expression in vascular endothelium. Proc Natl Acad Sci U S A, 1994. 91(11): p. 4678-82.

50. Ziegelstein, R.C., et al., Cytosolic alkalinization of vascular endothelial cells produced by an abrupt reduction in fluid shear stress. Circ Res, 1998. 82(7): p. 803-9.

51. Chappell, D.C., et al., Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium. Circ Res, 1998. 82(5): p. 532-9.

Shear stress as a molding force was recognized over 100 years ago; the embryologist Thoma described the relationship between the diameter of an artery and its blood flow velocity (14). Any sustained deviation from that relationship initiates processes of either growth or atrophy. A sustained increase of fluid shear stress leads to activation of the endothelium.

Activation of the endothelium

It is presently not well enough known how the stimulus of increased shear stress is transmitted from the endothelial cell membrane to the nucleus, where it initiates the transcriptional activity of a number of genes (12), partially via a protein that binds to the shear stress responsive element that is present in the promotor of several genes (NOS, PDGF, MCP-1). The first step in the activation of the endothelium is the opening of chloride channels that are also responsible for the volume control of endothelial cells. Characteristically stress-activated endothelium appears swollen in scanning electron microscopic images (15). Adhesion molecules are upregulated (4), and the conditions are perfect for the adhesion and invasion of circulating cells.


4. Chappell, D. C., S. E. Varner, R. M. Nerem, R. M. Medford, and R. W. Alexander. Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium. Circ. Res. 82: 532–539, 1998.

12. Shyy, Y.-J., H.-J. Hsieh, S. Usami, and S. Chien. Fluid shear stress induces a biphasic response of human monocyte chemotactic protein 1 expression in vascular endothelium. Proc. Natl. Acad. Sci. USA 91: 4678–4682, 1994.

14. Yancopoulos, G. D., M. Klagsbrun, and J. Folkman: Vasculogenesis, angiogenesis, and growth factors: ephrins enter the fray at the border. Cell 93: 661–664, 1998.

15. Ziegelstein, R. C., P. S. Blank, L. Cheng, and M. C. Capogrossi. Cytosolic alkalinization of vascular endothelial cells produced by an abrupt reduction in fluid shear stress. Circ. Res. 82: 803–809, 1998.

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Ein Verweis auf die Quelle fehlt.

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[8.] Haw/Fragment 012 08 - Diskussion
Bearbeitet: 20. October 2014, 22:07 WiseWoman
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1.3.6. Therapeutic arteriogenesis

In previous studies, Ito, W.D., et al., showed that chronic intra-arterial infusion of MCP-1 greatly increased the development of arterial collateral blood vessels (arteriogenesis) after FAO[7, 60]. These collaterals were more numerous on angiograms, and their ability to conduct blood had increased by six fold. (Fig. 1.3., A and B) The histological appearance of these typical corkscrew vessels was that of muscular arteries[20].

Therapeutic arteriogenesis

In previous studies we showed that chronic intra-arterial infusion of MCP-1 greatly increased the development of arterial collateral blood vessels (arteriogenesis) after femoral artery occlusion (6, 7). These collaterals were more numerous on angiograms, and their ability to conduct blood had increased by sixfold (Fig. 1, A and B). The histological appearance of these typical corkscrew vessels was that of muscular arteries.

Anmerkungen

Ein Verweis auf die Quelle fehlt hier. Man findet ihn auf der nächsten Seite.


"FAO" statt "femoral arterial occlusion"; "six fold" statt "sixfold". Übernahme der referenzierten Bilder aus Quelle:HAW/Buschmann and Schaper 1999 mit komplett plagierter Bildunterschrift.

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[9.] Haw/Fragment 006 10 - Diskussion
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In the case of a sudden arterial occlusion or a slowly progressing stenosis, a steep pressure gradient develops along the shortest path within the interconnecting network that increases the blood flow velocity and FSS in these vessels. The effect of this sustained increase in shear is the upregulation of distinct processes in the collateral arteries. In the case of a sudden arterial occlusion or a slowly progressing stenosis, a steep pressure gradient along the shortest path within the interconnecting network develops that increases the blood flow velocity and hence fluid shear stress in these vessels, which now assume the new function as “collaterals” [normal femoral artery blood flow 4.8 x 10-3 dyn/cm2; blood flow via anastomoses (occlusion) 889 x 10-3 dyn/cm2]. The effect of this sustained increase in shear is the upregulation of distinct processes in the collateral arteries.
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[10.] Haw/Fragment 005 01 - Diskussion
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Haw 05a diss.png

The equation that already includes blood viscosity (η) and the internal radius of a vessel (R), demonstrates that increased blood flow (Q) will directly result in increased FSS (τ)[9]. Furthermore, the wall of the collateral arteriole is influenced by pressure-related forces like longitudinal-, circumferential-, and radial wall stresses.


9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58.

Haw 05a source.png

The equation that already includes blood viscosity (η) and the internal radius of a vessel (R), demonstrates that increased blood flow (Q) will directly result in increased FSS (τ).8 Furthermore, the wall of the collateral arteriole is influenced by pressure-related forces like longitudinal-, circumferential-, and radial wall stresses.


8. Cox R. Physiology and hemodynamics of the macrocirculation. In: Stehbens W, eds. Hemodynamics and the Blood Vessel Wall. Springfield, Ill: Charles C. Thomas; 1979:75–156.

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[11.] Haw/Fragment 004 25 - Diskussion
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The collateral vessel wall is now exposed to various pronounced mechanical forces: increased blood flow directly augments FSS, i.e., the viscous drag that flowing blood exerts on the endothelial lining. Assuming Newtonian fluid dynamics, FSS can be estimated using the following equation: Hence, the collateral vessel wall is now exposed to various pronounced mechanical forces: increased blood flow directly augments fluid shear stress (FSS), ie, the viscous drag that flowing blood exerts on the endothelial lining. Assuming Newtonian fluid dynamics, FSS can be estimated using the following equation:
Anmerkungen

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[12.] Haw/Fragment 015 02 - Diskussion
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After peripheral artery occlusion in rabbits and mice, arteriogenesis proceeds much faster than angiogenesis because of a structural dilatation of pre-existing collateral vessels followed by mitosis of all vascular cell types, which restores resting blood flow within 3 days. Recovery of dilatory reserve (maximal flow) takes longer[20]. The slower angiogenesis is unable to significantly restore flow even if angiogenesis reduces the minimal terminal resistance of the entire chain of resistors by new capillaries in parallel. Future therapeutic efforts should be directed at stimulating arteriogenesis.

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

After peripheral artery occlusion in rabbits and mice, arteriogenesis proceeds much faster than angiogenesis because of a structural dilatation of preexisting collateral vessels followed by mitosis of all vascular cell types, which restores resting blood flow within 3 days. Recovery of dilatory reserve (maximal flow) takes longer. The slower angiogenesis is unable to significantly restore flow even if angiogenesis reduces the minimal terminal resistance of the entire chain of resistors by new capillaries in parallel. Future therapeutic aims should be directed at stimulating arteriogenesis.
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[13.] Haw/Fragment 011 01 - Diskussion
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[This is followed by an upregulation of] the expression and activity of the MMPs that digest the matrix and provide the space for new cells and enable SMCs to migrate toward the intima. Many SMCs of the old media undergo apoptosis and are replaced by new ones. Those that proliferate change their phenotype and lose most of their contractile material, which is replaced by endoplasmic reticulum (ER) and free ribosomes, an indication of their synthetic activity[18, 55]. The loss of the contractile phenotype is ascribed to the combined activities of protein kinase G, activin, and regulators of G protein signaling-5 (RGS-5). In addition to actin and myosin, desmin and calponin are downregulated and fibronectin is upregulated[66]. In general, protein synthesis in SMCs switches to an embryonic pattern. Because the thickening of the vessel wall occurs under markedly increased tangential wall stress, the intercellular connections and the communication between cells change. The remodelling process of large collaterals is finally characterized by the significant increase in length (tortuosity) and by the formation of a substantial intima (Fig. 1.3.)[21]. At very late stages, the intima disappears in mature collaterals, probably because the longitudinal muscle had assumed first a helical and later a circumferential orientation. In very small animals, like mice, neither intima formation nor pruning is observed, most probably because the increase in new tissue mass is so small that remodelling processes are not required[20]. However, already in the rabbit a sizeable intima is seen in hindlimb collaterals sometime after FAO. It is tempting to speculate that collateral arteries develop from the inside out using the intima as a platform; this is the incubator where the growth factors are produced, where the MMPs and other proteases are activated, and where the SMCs migrate to and then proliferate, thereby weakening the media from which they leave, producing the bulge of later tortuosity[20].

18. Scholz, D., et al., Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J Mol Cell Cardiol, 2002. 34(7): p. 775-87.

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

21. Buschmann, I. and W. Schaper, Arteriogenesis Versus Angiogenesis: Two Mechanisms of Vessel Growth. News Physiol Sci, 1999. 14: p. 121-125.

55. Scholz, D., et al., Ultrastructure and molecular histology of rabbit hind-limb collateral artery growth (arteriogenesis). Virchows Arch, 2000. 436(3): p. 257-70.

66. Cai, W.J., et al., Remodeling of the adventitia during coronary arteriogenesis. Am J Physiol Heart Circ Physiol, 2003. 284(1): p. H31-40.

This is followed by an upregulation of the expression and activity of the MMPs that digest the matrix and provide the space for new cells and enable SMCs to migrate toward the intima. Many SMCs of the old media die an apoptotic death and are replaced by new ones. Those that proliferate change their phenotype and lose most of their contractile material, which is replaced by endoplasmic reticulum and free ribosomes, an indication of their synthetic activity.11,12 The loss of the contractile phenotype is ascribed to the combined activities of protein kinase G, activin, and RGS-5. In addition to actin and myosin, desmin and calponin are downregulated and fibronectin is upregulated.82 In general, protein synthesis in SMCs switches to an embryonic pattern.

[Seite 1149]

Because the thickening of the vessel wall occurs under markedly increased tangential wall stress, the intercellular connections and the communication between cells change. [...] The remodelling process of large collaterals is finally characterized by the significant increase in length (tortuosity) and by the formation of a substantial intima (Figure 3). At very late stages, the intima disappears in mature collaterals, probably because the longitudinal muscle had assumed first a helical and later a circumferential orientation. In very small animals, like mice, neither intima formation nor pruning is observed, most probably because the increase in new tissue mass is so small that remodelling processes are not required. However, already in the rabbit a sizeable intima is seen in hindlimb collaterals sometime after femoral artery occlusion.

It is tempting to speculate that collateral arteries develop from the inside out using the intima as a platform; this is the incubator where the growth factors are produced, where the MMPs and other proteases are activated, and where the SMCs migrate to and then proliferate, thereby weakening the media from which they leave, producing the bulge of later tortuosity.


11. Scholz D, Ito W, Fleming I, Deindl E, Sauer A, Babiak A, Bühler A, Wiesnet M, Busse R, Schaper J, Schaper W. Ultrastructure and molecular histology of rabbit hindlimb collateral artery growth. Virchows Arch. 2000;436:257–270.

12. Scholz D, Ziegelhoeffer T, Helisch A, Wagner S, Friedrich C, Podzuweit T, Schaper W. Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J Mol Cell Cardiol. 2002;34: 775–787.

82. Cai W-J, Koltai S, Kocsis E, Scholz D, Kostin S, Luo X, Schaper W, Schaper J. Remodeling of the adventitia during coronary arteriogenesis. Am J Physiol. 2003;284:H31–H40.

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Mature collateral vessels differ only in minor histological aspects from normal arteries of the conductance type: they are muscular and contain more collagen and exhibit transiently, during the growth process, a significant intima consisting of smooth muscle cells in the synthetic and proliferative phenotype. Mature collateral vessels differ only in minor histological aspects from normal arteries of the conductance type: they are muscular and contain more collagen and exhibited transiently during the growth process a significant intima consisting of smooth muscle cells in the synthetic and proliferative phenotype.
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[15.] Haw/Fragment 003 04 - Diskussion
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Growth of collateral blood vessels (arteriogenesis) is potentially able to preserve structure and function of limbs and organs after occlusion of a major artery. The success of the remodeling process depends on the following conditions: (1) existence of an arteriolar network that connects the preocclusive with the postocclusive microcirculation; (2) activation of the arteriolar endothelium by elevated fluid shear stress; (3) invasion (but not incorporation) of bone marrow–derived cells; and (4) proliferation of endothelial and smooth muscle cells[9].

9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58.

Growth of collateral blood vessels (arteriogenesis) is potentially able to preserve structure and function of limbs and organs after occlusion of a major artery. The success of the remodeling process depends on the following conditions: (1) existence of an arteriolar network that connects the preocclusive with the postocclusive microcirculation; (2) activation of the arteriolar endothelium by elevated fluid shear stress; (3) invasion (but not incorporation) of bone marrow–derived cells; and (4) proliferation of endothelial and smooth muscle cells.
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[However, they differ markedly in their] anatomical appearance: they are sometimes excessively tortuous[13, 25]. In the re-entry region, they join up with the distal part of the occluded artery at nonphysiological angles, which adds to the resistance to flow. Collateral arteries can develop relatively quickly provided a pre-existent network of arterioles had existed before occlusion of the artery but they can also quickly regress when the occluded artery is opened up again[22]. This may also be the case when the subtended tissue had atrophied or is not used to full potential like in the peripheral circulation supplying the muscles of the leg. Most often, an occluded artery is not replaced by one single large collateral vessel but rather by several smaller ones. But this arrangement is inefficient because according to the Poiseuille’s Law the energy losses created by the resistance of the contributing vessels are additive[9]. During the course of collateral artery development many of the smaller contributing vessels regress, whereas the larger ones increase in diameter and make the system more efficient. However, no ideal adaptation is reached. At optimal conditions (no tissue loss after arterial occlusion), collateral vessels recover only approximately 40% of the maximal conductance (flow at a given blood pressure at maximal vasodilatation). This was shown for the canine heart and for the peripheral circulation in pigs, rabbits, and mice[7, 26].

7. Ito, W.D., et al., Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am J Physiol, 1997. 273(3 Pt 2): p. H1255-65.

9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58.

13. Schaper, W., Tangential wall stress as a molding force in the development of collateral vessels in the canine heart. Experientia, 1967. 23(7): p. 595-6.

22. Fulton, W.F., The Time Factor in the Enlargement of Anastomoses in Coronary Artery Disease. Scott Med J, 1964. 9: p. 18-23.

25. Korff, T., K. Aufgebauer, and M. Hecker, Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation, 2007. 116(20): p. 2288-97.

26. Kumada, T., et al., Comparison of postpacing and exercise-induced myocardial dysfunction during collateral development in conscious dogs. Circulation, 1982. 65(6): p. 1178-85.

However, they differ markedly in their anatomical appearance: they are sometimes excessively tortuous.1 In the reentry region, they join up with the distal part of the occluded artery at nonphysiological angles, which adds to the resistance toward flow. Collateral arteries can develop relatively quickly provided a preexistent network of arterioles had existed before occlusion of the artery but they can also quickly regress when the occluded artery is opened up again.2 This may also be the case when the subtended tissue had atrophied or is not used to full potential like in the peripheral circulation supplying the muscles of the leg. Most often, an occluded artery is not replaced by one single large collateral vessel but rather by several smaller ones. But this arrangement is inefficient because according to the Poiseuille’s Law the energy losses created by the resistance of the contributing vessels are additive. During the course of collateral artery development many of the smaller contributing vessels regress, whereas the larger ones increase in diameter and make the system more efficient. However, no ideal adaptation is reached. At optimal conditions (no tissue loss after arterial occlusion), collateral vessels recover only approximately 40% of the maximal conductance (flow at a given blood pressure at maximal vasodilatation). This was shown for the canine heart and for the peripheral circulation in pigs, rabbits, and mice.3–5

1. Schaper W. The Collateral Circulation of the Heart. Amsterdam London: Elsevier North Holland Publishing Company; 1971.

2. Fulton WFM. The time factor in the enlargement of anastomoses in coronary artery disease. Scot Med J. 1964;9:18–23.

3. Kumada T, Gallagher KP, Battler A, White F, Kemper WS, Ross Jr J. Comparison of postpacing and exercise-induced myocardial dysfunction during collateral development in conscious dogs. Circulation. 1982;65:1178–1185.

4. Ito WD, Arras M, Scholz D, Winkler B, Htun P, Schaper W. Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am J Physiol. 1997;273:H1255–H1265.

5. Elsaesser H, Sauer A, Friedrich C, Helisch A, Luttun A, Carmeliet P, Scholz D, Schaper W. Bone marrow transplants abolish inhibition of arteriogenesis in placenta growth factor k.o. mice. J Mol Cell Cardiol. 2000;32:A29. Abstract

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[17.] Haw/Fragment 006 01 - Diskussion
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The pressure derived pulsatile stretch is also discussed[25, 36, 37], and the transcription factor- activator protein 1 (AP-1) is the molecular transducer. However, AP-1 is also activated by FSS[38], Pulsatile stretch can only be tested acutely and in vitro with its inherent limits. Cultured endothelium under stretch alters translation and transcription of growth factors and changes the sensitivity to cytokines[11, 39, 40]. If pulsatile stretch is a molding force, it must be demonstrated that in collateral growth pulsatile stretch is higher than the physiological levels in normal small arteries. Furthermore, in arterial occlusion the intravascular pressure downstream from the occlusion is much lower than the systemic arterial pressure[8].

8. Schaper, W., Collateral circulation: past and present. Basic Res Cardiol, 2009. 104(1): p. 5-21.

11. Eitenmuller, I., et al., The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res, 2006. 99(6): p. 656-62.

25. Korff, T., K. Aufgebauer, and M. Hecker, Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation, 2007. 116(20): p. 2288-97.

36. Lehoux, S., et al., Differential regulation of vascular focal adhesion kinase by steady stretch and pulsatility. Circulation, 2005. 111(5): p. 643-9.

37. Popp, R., I. Fleming, and R. Busse, Pulsatile stretch in coronary arteries elicits release of endothelium-derived hyperpolarizing factor: a modulator of arterial compliance. Circ Res, 1998. 82(6): p. 696-703.

38. Miyagi, M., et al., Activator protein-1 mediates shear stress-induced prostaglandin d synthase gene expression in vascular endothelial cells. Arterioscler Thromb Vasc Biol, 2005. 25(5): p. 970-5.

39. Busse, R. and I. Fleming, Pulsatile stretch and shear stress: physical stimuli determining the production of endothelium-derived relaxing factors. J Vasc Res, 1998. 35(2): p. 73-84.

40. Demicheva, E., M. Hecker, and T. Korff, Stretch-induced activation of the transcription factor activator protein-1 controls monocyte chemoattractant protein-1 expression during arteriogenesis. Circ Res, 2008. 103(5): p. 477-84.

However, pressure derived pulsatile stretch is also discussed [83, 88, 110] and the transcription factor AP-1 is the molecular transducer. However, AP-1 is also activated by FSS [96]. Pulsatile stretch can only be tested acutely and in vitro with its inherent limits. Cultured endothelium under stretch alters translation and transcription of growth factors and changes the sensitivity to cytokines[14, 32, 110]. If pulsatile stretch is a molding force it must be demonstrated that in collateral growth pulsatile stretch is higher than the physiological levels in normal small arteries. Furthermore, in arterial occlusion the intravascular pressure downstream from the occlusion (and hence in the receiving end of the collateral arcade) is much lower than the systemic arterial pressure [...]

14. Busse R, Fleming I (1998) Pulsatile stretch and shear stress: physical stimuli determining the production of endothelium-derived relaxing factors. J Vasc Res 35:73–84

32. Demicheva E, Hecker M, Korff T (2008) Stretch-induced activation of the transcription factor activator protein-1 controls monocyte chemoattractant protein-1 expression during arteriogenesis. Circ Res (in press)

83. Korff T, Aufgebauer K, Hecker M (2007) Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation 116:2288–2297

88. Lehoux S, Esposito B, Merval R, Tedgui A (2005) Differential regulation of vascular focal adhesion kinase by steady stretch and pulsatility. Circulation 111:643–649

96. Miyagi M, Miwa Y, Takahashi-Yanaga F, Morimoto S, Sasaguri T (2005) Activator protein-1 mediates shear stress-induced prostaglandin d synthase gene expression in vascular endothelial cells. Arterioscler Thromb Vasc Biol 25:970–975

110. Popp R, Fleming I, Busse R (1998) Pulsatile stretch in coronary arteries elicits release of endothelium-derived hyperpolarizing factor: a modulator of arterial compliance. Circ Res 82:696–703

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[18.] Haw/Fragment 005 06 - Diskussion
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It is generally assumed that a physical stimulus starts the remodeling process whereby increased pressure leads to increased wall thickness and increased flow to increased arterial diameter. Pressure-dependent forces are by far the highest in magnitude and they affect both the endothelium as well as the muscular media. It is therefore logical to assume that these are important factors for remodeling[13, 25]. However, in collateral growth with its pressure gradient driven increase in flow, the much weaker FSS, which the viscous drag of flowing blood exerts on the endothelial [lining, is the determining force[11, 29-35].]

11. Eitenmuller, I., et al., The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res, 2006. 99(6): p. 656-62.

13. Schaper, W., Tangential wall stress as a molding force in the development of collateral vessels in the canine heart. Experientia, 1967. 23(7): p. 595-6.

25. Korff, T., K. Aufgebauer, and M. Hecker, Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation, 2007. 116(20): p. 2288-97.

29. Ben Driss, A., et al., Arterial expansive remodeling induced by high flow rates. Am J Physiol, 1997. 272(2 Pt 2): p. H851-8.

30. Buus, C.L., et al., Smooth muscle cell changes during flow-related remodeling of rat mesenteric resistance arteries. Circ Res, 2001. 89(2): p. 180-6.

31. Girard, P.R. and R.M. Nerem, Shear stress modulates endothelial cell morphology and F-actin organization through the regulation of focal adhesion-associated proteins. J Cell Physiol, 1995. 163(1): p. 179-93.

32. Langille, B.L., Remodeling of developing and mature arteries: endothelium, smooth muscle, and matrix. J Cardiovasc Pharmacol, 1993. 21 Suppl 1: p. S11-7.

33. Resnick, N., et al., Fluid shear stress and the vascular endothelium: for better and for worse. Prog Biophys Mol Biol, 2003. 81(3): p. 177-99.

34. Tronc, F., et al., Role of NO in flow-induced remodeling of the rabbit common carotid artery. Arterioscler Thromb Vasc Biol, 1996. 16(10): p. 1256-62.

35. Tzima, E., et al., A mechanosensory complex that mediates the endothelial cell response to fluid shear stress. Nature, 2005. 437(7057): p. 426-31.

It is generally assumed that a physical stimulus starts the remodeling process whereby increased pressure leads to increased wall thickness and increased flow to increased arterial diameter. Pressure-dependent forces are by far the highest in magnitude and they affect both the endothelium as well as the muscular media. It is therefore logical to assume that these are important factors for remodeling [83, 121, 122]. [...] However, in collateral growth with its pressure gradient driven increase in flow the much weaker FSS, which the viscous drag of flowing blood exerts on the endothelial lining, is the determining force [8, 17, 35, 49, 85, 114, 142, 145, 149].

8. Ben Driss A, Benessiano J, Poitevin P, Levy BI, Michel JB (1997) Arterial expansive remodeling induced by high flow rates. Am J Physiol 272:H851–H858

17. Buus CL, Pourageaud F, Fazzi GE, Janssen G, Mulvany MJ, De Mey JG (2001) Smooth muscle cell changes during flow-related remodeling of rat mesenteric resistance arteries. Circ Res 89:180–186

35. Eitenmuller I, Volger O, Kluge A, Troidl K, Barancik M, Cai WJ, Heil M, Pipp F, Fischer S, Horrevoets AJ, Schmitz-Rixen T, Schaper W (2006) The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res 99:656–662

49. Girard PR, Nerem RM (1995) Shear stress modulates endothelial cell morphology and F-actin organization through the regulation of focal adhesion- associated proteins. J Cell Physiol 163:179–193

83. Korff T, Aufgebauer K, Hecker M (2007) Cyclic stretch controls the expression of CD40 in endothelial cells by changing their transforming growth factor-beta1 response. Circulation 116:2288–2297

85. Langille BL (1993) Remodeling of developing and mature arteries: endothelium, smooth muscle, and matrix. J Cardiovasc Pharmacol 21(Suppl 1):S11–S17

114. Resnick N, Yahav H, Shay-Salit A, Shushy M, Schubert S, Zilberman LC, Wofovitz E (2003) Fluid shear stress and the vascular endothelium: for better and for worse. Prog Biophys Mol Biol 81:177–199

121. Schaper W (1967) Tangential wall stress as a molding force in the development of collateral vessels in the canine heart. Experientia 23:595– 596

122. Schaper W (1971) The collateral circulation of the heart. Elsevier North Holland Publishing Company, Amsterdam

142. Thoma R (1893) Untersuchungen über die Histogenese und Histomechanik des Gefäßsystems. F.Enke, Stuttgart

145. Tronc F, Wassef M, Esposito B, Henrion D, Glagov S, Tedgui A (1996) Role of NO in flow-induced remodeling of the rabbit common carotid artery. Arterioscler Thromb Vasc Biol 16:1256–1262

149. Tzima E, Irani-Tehrani M, Kiosses WB, Dejana E, Schultz DA, Engelhardt B, Cao G, DeLisser H, Schwartz MA (2005) A mechanosensory complex that mediates the endothelial cell response to fluid shear stress. Nature 437:426–431

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Both large areas (a full torso) and small areas (part of a finger) can be scanned, enabling the blood flow to be mapped and colour coded images of the blood flow displayed. Regions of interest can be defined and statistical data can be calculated and recorded.

Single point measurements give a high temporal resolution (40Hz data rates are typical) enabling rapid blood flow changes to be recorded, whereas the laser Doppler imager can provide spatial information and has the ability to average blood flow measurements over large areas. Fibre optic systems can measure at tissue sites not easily accessible to a laser beam. For example measurements in brain tissue, mouth, gut, colon, muscle and bone.

5.3. The definition of perfusion units

The term commonly used to describe blood flow measured by the laser Doppler technique is ‘flux’: a quantity proportional to the product of the average speed of the blood cells and their number concentration (often referred to as blood volume). This is expressed in arbitrary ‘perfusion units’ and is calculated using the first moment of the power spectral density.

Both large areas (a full torso) and small areas (part of a finger) can be scanned enabling the blood flow to be mapped and colour coded images of the blood flow displayed. Regions of interest can be defined and statistical data calculated and recorded.

[Seite 3]

Single point measurements give a high temporal resolution (40Hz data rates are typical) enabling rapid blood flow changes to be recorded, whereas the laser Doppler imager can provide spatial information and has the ability to average blood flow measurements over large areas. Fibre optic systems can measure at tissue sites not easily accessible to a laser beam. For example measurements in brain tissue, mouth, gut, colon, muscle and bone.

[...]

Definitions

The term commonly used to describe blood flow measured by the laser Doppler technique is ‘flux’: a quantity proportional to the product of the average speed of the blood cells and their number concentration (often referred to as blood volume). This is expressed in arbitrary ‘perfusion units’ and is calculated using the first moment of the power spectral density.

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Laser Doppler is a standard technique for the non-invasive blood flow monitoring and measurement of blood flow in the microcirculatory system. The strength of the technique is in looking at changes in flow - either over time or differences in flow over an area of skin or other exposed tissue.

5.2. Operating principles

The laser Doppler technique measures blood flow in the very small blood vessels of the microvasculature, such as the low-speed flows associated with nutritional blood flow in capillaries close to the skin surface and flow in the underlying arterioles and venules involved in regulation of skin temperature. The tissue thickness sampled is typically 1mm, the capillary diameters 10 microns and the velocity spectrum measurement typically 0.01 to 10mm/s.

The technique depends on the Doppler principle whereby low power light from a monochromatic stable laser, e.g. a helium neon gas laser or a single mode laser diode, incident on tissue is scattered by moving red blood cells and as a consequence is frequency broadened. The frequency broadened light, together with laser light scattered from static tissue, is photo-detected and the resulting photocurrent processed to provide a blood flow measurement. Please note, where laser light is scattered for tissue with a low red blood cell concentration, the average Doppler frequency shift is proportional to the average speed of red blood cells.

Laser light can be directed to the tissue surface either via an optic fibre (Fig.1.8.a) or as a light beam (Fig.1.8.b). For ‘fibre optic’ monitors (LDF instruments) the optic fibre terminates in an optic probe which can be attached to the tissue surface. One or more light collecting fibres also terminate in the probe head and these fibres transmit a proportion of the scattered light to a photo-detector and the electronic signal processing [system.]

Laser Doppler is a standard technique for the non-invasive blood flow monitoring and measurement of blood flow in the microcirculation. The strength of the technique is in looking at changes in flow - either over time or differences in flow over an area of skin or other exposed tissue.

[...]

Operating Principles

The laser Doppler technique measures blood flow in the very small blood vessels of the microvasculature, such as the low-speed flows associated with nutritional blood flow in capillaries close to the skin surface and flow in the underlying arterioles and venules involved in regulation of skin temperature. The tissue thickness sampled is typically 1mm, the capillary diameters 10 microns and the velocity spectrum measurement typically 0.01 to 10mm/s. The technique depends on the Doppler principle whereby low power light from a monochromatic stable laser (a), e.g. a Helium Neon gas laser or a single mode laser diode, incident on tissue is scattered by moving red blood cells and as a consequence is frequency broadened (b). The frequency broadened light, together with laser light scattered from static tissue, is photodetected and the resulting photocurrent processed to provide a blood flow measurement. Please note, where laser light is scattered for tissue with a low red blood cell concentration the average Doppler frequency shift is proportional to the average speed of red blood cells.

[Seite 2]

Laser light can be directed to the tissue surface either via an optic fibre (c) or as a light beam (d). For ‘fibre optic’ monitors (LDF instruments) the optic fibre terminates in an optic probe which can be attached to the tissue surface. One or more light collecting fibres also terminate in the probe head and these fibres transmit a proportion of the scattered light to a photodetector and the signal processing electronics.

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The presence of these native collaterals, which may not be utilized to provide perfusion under normal conditions, varies widely among species and also within individuals. However, these vessels have the ability to dramatically increase the lumen by growth so as to provide enhanced perfusion to the jeopardized ischemic regions. In case of chronic or acute occlusion of a major artery, collateral arteries can relieve the ensuing harmful effects in many regions of the body (hindlimb, heart, brain and kidney). It is important to recognize that this process is not a passive dilatation but one of active proliferation and remodeling. Under normal flow conditions and depending on the pressure gradient between the interconnecting arterial networks there is only minimal net forward flow, but small amounts of flow may oscillate within the network. The presence of these native collaterals, which may not be utilized to provide perfusion under normal conditions, varies widely among species and also within individuals. However, these vessels have the ability to dramatically increase the lumen by growth so as to provide enhanced perfusion to the jeopardized ischemic regions. In case of chronic or acute occlusion of a major artery, collateral arteries can ameliorate the ensuing detrimental effects in many regions of the body (hindlimb, heart, brain, kidney). It is important to recognize that this process is not a passive dilatation but one of active proliferation and remodeling. Under normal flow conditions and depending on the pressure gradient between the interconnecting arterial networks there is only minimal net forward flow, but small amounts of flow may oscillate within the network.
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Cardiovascular diseases are the number one cause of death globally[104]. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.

104. Murray, C.J. and A.D. Lopez, Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet, 1997. 349(9063): p. 1436-42.

Cardiovascular diseases are the number one cause of death globally1. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.

1. World Health Organization. in Fact sheet No. 317 Feb. 2007 (World Health Organization, 2007) (http://www.who.int/mediacentre/factsheets/fs317/en/index.html).

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The Doppler signal is linearly proportional to perfusion of the upper 200–300 μm of the skin[131]. Tissue perfusion is quantified in regions of interest (ROI) defined in the limbs relative to the contralateral, non-ligated side and can be displayed as color-coded images[132]. Perfusion measurements obtained from ROIs of thighs are confounded by fur, skin pigmentation and motion artifacts from the abdomen and have been shown not to correlate with limb perfusion[132]. We therefore take LDI measurements from the feet, which correlate with other measures of limb perfusion[18, 133].

18. Scholz, D., et al., Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J Mol Cell Cardiol, 2002. 34(7): p. 775-87.

131. Jakobsson, A. and G.E. Nilsson, Prediction of sampling depth and photon pathlength in laser Doppler flowmetry. Med Biol Eng Comput, 1993. 31(3): p. 301-7.

132. Chalothorn, D., et al., Collateral density, remodeling, and VEGF-A expression differ widely between mouse strains. Physiol Genomics, 2007. 30(2): p. 179-91.

133. Helisch, A., et al., Impact of mouse strain differences in innate hindlimb collateral vasculature. Arterioscler Thromb Vasc Biol, 2006. 26(3): p. 520-6.

The Doppler signal is linearly proportional to perfusion of the upper 200–300 μm of the skin22. Tissue perfusion is quantified in regions of interest (ROI) defined in the limbs relative to the contralateral, non-ligated side and can be displayed as color-coded images23. Perfusion measurements obtained from ROIs of thighs are confounded by fur, skin pigmentation and motion artifacts from the abdomen and have been shown not to correlate with limb perfusion23. We therefore

[Seite 1739]

take LDI measurements from the feet, which correlate with other measures of limb perfusion15,24.


15. Scholz, D. et al. Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J. Mol. Cell. Cardiol. 34, 775–787 (2002).

22. Jakobsson, A. & Nilsson, G.E. Prediction of sampling depth and photon path length in laser Doppler flowmetry. Med. Biol. Eng. Comput. 31, 301–307 (1993).

23. Chalothorn, D., Clayton, J.A., Zhang, H., Pomp, D. & Faber, J.E. Collateral density, remodeling, and VEGF-A expression differ widely between mouse strains. Physiol. Genomics 30, 179–191 (2007).

24. Helisch, A. et al. Impact of mouse strain differences in innate hindlimb collateral vasculature. Arterioscler. Thromb. Vasc. Biol. 26, 520–526 (2006).

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Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.
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Cardiovascular diseases are the number one cause of death globally[104]. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.

104. Murray, C.J. and A.D. Lopez, Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet, 1997. 349(9063): p. 1436-42.

Cardiovascular diseases are the number one cause of death globally1. Arteries are the key vessels affected in cardiovascular diseases and the study of mechanisms of arterial growth and repair are, therefore, of fundamental interest.

1. World Health Organization. in Fact sheet No. 317 Feb. 2007 (World Health Organization, 2007) (http://www.who.int/mediacentre/factsheets/fs317/en/index.html).

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Angiogenesis, i.e., the sprouting of capillaries from the pre-existing vasculature, is mainly initiated by hypoxia in ischemic tissue[3]. These newly formed capillaries consist of endothelial tubes lacking proper wall structures. Angiogenesis alone has a limited capacity to increase perfusion of the surrounding ischemic tissue.

3. Carmeliet, P., Mechanisms of angiogenesis and arteriogenesis. Nat Med, 2000. 6(4): p. 389-95.

Angiogenesis, i.e., the sprouting of capillaries from the pre-existing vasculature, is mainly initiated by hypoxia in ischemic tissue4. These newly formed capillaries consist of endothelial tubes lacking proper wall structures. Angiogenesis alone has a limited capacity to increase perfusion of the surrounding ischemic tissue.

4. Carmeliet, P. Mechanisms of angiogenesis and arteriogenesis. Nat. Med. 6, 389–395 (2000).

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[Arteriogenesis is defined as the enlargement of pre-existing collateral arteries and their remodelling into conductance vessels[8]. This process is driven by an] increased blood flow in collateral arteries leading to an increase in wall tension and fluid shear stress[9-11]. Specific arterial signaling pathways, angiogenic growth factors, as well as resident cells in the vessel wall and circulating cells participate in this complex biological process of luminal expansion and wall growth[12-17]. It is important to note that arteriogenesis is the key mechanism to enhance perfusion and is, thus, critical for the rescue of ischemic organs[18, 19].

8. Schaper, W., Collateral circulation: past and present. Basic Res Cardiol, 2009. 104(1): p. 5-21.

9. Heil, M. and W. Schaper, Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ Res, 2004. 95(5): p. 449-58.

10. Heil, M., et al., Arteriogenesis versus angiogenesis: similarities and differences. J Cell Mol Med, 2006. 10(1): p. 45-55.

11. Eitenmuller, I., et al., The range of adaptation by collateral vessels after femoral artery occlusion. Circ Res, 2006. 99(6): p. 656-62.

12. Limbourg, A., et al., Notch ligand Delta-like 1 is essential for postnatal arteriogenesis. Circ Res, 2007. 100(3): p. 363-71.

13. Schaper, W., Tangential wall stress as a molding force in the development of collateral vessels in the canine heart. Experientia, 1967. 23(7): p. 595-6.

14. Arras, M., et al., Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J Clin Invest, 1998. 101(1): p. 40-50.

15. Jacobi, J., et al., Adenoviral gene transfer with soluble vascular endothelial growth factor receptors impairs angiogenesis and perfusion in a murine model of hindlimb ischemia. Circulation, 2004. 110(16): p. 2424-9.

16. Kondoh, K., et al., Conduction performance of collateral vessels induced by vascular endothelial growth factor or basic fibroblast growth factor. Cardiovasc Res, 2004. 61(1): p. 132-42.

17. Ziegelhoeffer, T., et al., Bone marrow-derived cells do not incorporate into the adult growing vasculature. Circ Res, 2004. 94(2): p. 230-8.

18. Scholz, D., et al., Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J Mol Cell Cardiol, 2002. 34(7): p. 775-87.

19. Simons, M., Angiogenesis: where do we stand now? Circulation, 2005. 111(12): p. 1556-66.

Arteriogenesis, on the other hand, is defined as the enlargement of pre-existing collateral arteries and their remodelling to conductance vessels5. This process is driven by an increased blood flow in collateral arteries leading to an increase in wall tension and fluid shear stress6–8. Specific arterial signaling pathways, angiogenic growth factors, as well as resident cells in the vessel wall and circulating cells participate in this complex biological process of luminal expansion and wall growth9–14. It is important to note that arteriogenesis is the key mechanism to enhance perfusion and is, thus, critical for the rescue of ischemic organs15,16.

5. Schaper, W. Collateral circulation: past and present. Basic Res. Cardiol. 104, 5–21 (2009).

6. Heil, M. & Schaper, W. Influence of mechanical, cellular, and molecular factors on collateral artery growth (arteriogenesis). Circ. Res. 95, 449–458 (2004).

7. Heil, M., Eitenmuller, I., Schmitz-Rixen, T. & Schaper, W. Arteriogenesis versus angiogenesis: similarities and differences. J. Cell. Mol. Med. 10, 45–55 (2006).

8. Eitenmuller, I. et al. The range of adaptation by collateral vessels after femoral artery occlusion. Circ. Res. 99, 656–662 (2006).

9. Limbourg, A. et al. Notch ligand Delta-like 1 is essential for postnatal arteriogenesis. Circ. Res. 100, 363–371 (2007).

10. Schaper, W., Jageneau, A. & Xhonneux, R. The development of collateral circulation in the pig and dog heart. Cardiologia 51, 321–335 (1967).

11. Arras, M. et al. Monocyte activation in angiogenesis and collateral growth in the rabbit hindlimb. J. Clin. Invest. 101, 40–50 (1998).

12. Jacobi, J. et al. Adenoviral gene transfer with soluble vascular endothelial growth factor receptors impairs angiogenesis and perfusion in a murine model of hindlimb ischemia. Circulation 110, 2424–2429 (2004).

13. Kondoh, K. et al. Conduction performance of collateral vessels induced by vascular endothelial growth factor or basic fibroblast growth factor. Cardiovasc. Res. 61, 132–142 (2004).

14. Ziegelhoeffer, T. et al. Bone marrow-derived cells do not incorporate into the adult growing vasculature. Circ. Res. 94, 230–238 (2004).

15. Scholz, D. et al. Contribution of arteriogenesis and angiogenesis to postocclusive hindlimb perfusion in mice. J. Mol. Cell. Cardiol. 34, 775–787 (2002).

16. Simons, M. Angiogenesis: where do we stand now? Circulation 111, 1556–1566 (2005).

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[28.] Haw/Fragment 001 17 - Diskussion
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During embryonic development, blood vessels form de novo from angiogenic blood islands in a process termed vasculogenesis. This primary plexus extends by capillary sprouting and eventually remodels into a highly organized network of capillaries, arteries and veins[4]. The postnatal vascular system is critical for maintaining homeostasis and adapts readily to environmental cues and physiological or pathological conditions[5]. This adaptation comprises two different and characteristic responses, angiogenesis and arteriogenesis.

4. Adams, R.H. and K. Alitalo, Molecular regulation of angiogenesis and lymphangiogenesis. Nat Rev Mol Cell Biol, 2007. 8(6): p. 464-78.

5. Carmeliet, P., Angiogenesis in health and disease. Nat Med, 2003. 9(6): p. 653-60.

During the embryonic development, blood vessels form de novo from angiogenic blood islands in a process termed vasculogenesis. This primary plexus extends by capillary sprouting and eventually remodels into a highly organized network of capillaries, arteries and veins2. The postnatal vascular system is critical for maintaining homeostasis and adapts readily to environmental cues and physiological or pathological conditions3. This adaptation comprises two different and characteristic responses, angiogenesis and arteriogenesis.

2. Adams, R.H. & Alitalo, K. Molecular regulation of angiogenesis and lymphangiogenesis. Nat. Rev. Mol. Cell. Biol. 8, 464–478 (2007).

3. Carmeliet, P. Angiogenesis in health and disease. Nat. Med. 9, 653–660 (2003).

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1.3.5. Remodeling

After the acute phase of arteriogenesis that is dominated by the inflammatory events, remodelling begins (phase 2 of arteriogenesis), i.e., the much slower consolidation of the arterial structure after the final diameter was almost reached. A new elastic lamina is synthesized by the SMCs, and the rebuilding of the media and the formation of an intima begins with the downregulation of the tissue inhibitor of matrixmetalloproteinases (TIMP and MMP)[65].


65. Cai, W., et al., Altered balance between extracellular proteolysis and antiproteolysis is associated with adaptive coronary arteriogenesis. J Mol Cell Cardiol, 2000. 32(6): p. 997-1011

Remodelling

After the acute phase of arteriogenesis that is dominated by the inflammatory events, remodelling begins (phase 2 of arteriogenesis), ie, the much slower consolidation of the arterial structure after the final diameter was almost reached. A new elastic lamina is synthesized by the SMCs, and the rebuilding of the media and the formation of an intima begins with the downregulation of the tissue inhibitor of matrixmetalloproteinases (TIMP and MMP).80,81


80. Cai WJ, Vosschulte R, Koltai S, Kostin S, Schaper W, Schaper J. Extracellular proteolysis is involved in coronary collateral vessel development in dog. J Mol Cell Cardiol. 1997;29:A128.

81. Cai WJ, Vosschulte R, Afsah-Hedrij A, Koltai S, Koscic E, Scholz D, Kostin S, Schaper W, Schaper J. Altered balance between extracellular proteolysis and antiproteolysis is associated with adaptive coronary arteriogenesis. J Mol Cell Cardiol. 2000;32:997–1011.

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Studying vascular development or the mechanisms of neovascularisation (angiogenesis, arteriogenesis or vasculogenesis) and evaluating the effects of pro or antiangiogenic [strategies require complete and accurate analysis of the neoformed vascular network.] Studying vascular development or the mechanisms of neovascularisation (angiogenesis, arteriogenesis or vasculogenesis) and evaluating the effects of pro or antiangiogenic strategies require complete and accurate analysis of the neoformed vascular network.
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[31.] Haw/Fragment 056 01 - Diskussion
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Identification of markers of collateral growth could help in determining patient prognosis and predicting therapy response and maybe even lead to new, proarteriogenic therapies. Development of preclinical animal models is needed to test these methods, as extreme caution needs to be taken when extrapolating research in mice to the clinical setting. This will also enable further investigation of mechanisms, e.g., signaling molecules involved in collateral artery growth, extending our knowledge, and possibilities in therapeutic application. Future research will therefore involve investigation of the mechanisms behind the individual response to arteriogenesis. Identification of markers of collateral growth could help in determining patient prognosis and predicting therapy response and maybe even lead to new, proarteriogenic therapies.

[...] Development of preclinical animal models (preferably large animal models such as pigs) is needed to test these methods, as extreme caution needs to be taken when extrapolating research in mice to the clinical setting. This will also enable further investigation of mechanisms, e.g., signaling molecules involved in collateral artery growth, extending our knowledge, and possibilities in therapeutic application.

Future research will therefore involve investigation of the mechanisms behind the individual response to arteriogenesis and its relation to growth factor and cell therapy for the development of novel, therapeutic strategies.

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Cardiovascular diseases are the number one cause of death globally[104]. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients [who do not benefit from these treatment options.]

104. Murray, C.J. and A.D. Lopez, Global mortality, disability, and the contribution of risk factors: Global Burden of Disease Study. Lancet, 1997. 349(9063): p. 1436-42.

In fact, cardiovascular disorders are currently the leading cause of death globally [1]. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients who do not benefit from these treatment options.

1. World Health Organization (February 2007) Factsheet 317.

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Arteriogenesis (collateral vessel growth) is triggered by fluid shear stress in case of an arterial occlusion. It is an important focus in current cardiovascular research as it might provide new therapeutic opportunities. But the molecular mechanisms underlying arteriogenesis are not yet completely understood. Arteriogenesis (collateral vessel growth) is triggered by fluid shear stress in case of an arterial occlusion. It is an important focus in current cardiovascular research as it might provide new therapeutic opportunities. Although the molecular mechanisms underlying arteriogenesis are not yet completely understood, it has been shown that monocytes/macrophages and lymphocytes, in particular NK- and Tlymphocytes, play an important role in arteriogenesis.
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Although the participation of the gap junction in vascular function seems to be very complex, the development of connexin-knockout animals has been a great contribution to our understanding of how these proteins work in the vasculature. Although the participation of the gap junction in vascular function seems to be very complex, the development of connexin- knockout animals has been a great contribution to our understanding of how these proteins work in the vasculature.
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Interestingly, Pipp et al.[44], demonstrated the importance of FSS in arteriogenesis by means of a porcine ischemic hindlimb model with extremely high levels of collateral flow and FSS. Normally, during the later phases of arteriogenesis, FSS decreases as the collateral diameter increases so that FSS normalizes. This drop in FSS acts as a signal to arrest proliferation and as a result, prevents further collateral growth before an optimal adaptation is reached. Pipp and colleagues [44] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic factor in collateral growth.

44. Pipp, F., et al., Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hindlimb. Arterioscler Thromb Vasc Biol, 2004. 24(9): p. 1664-8.

Interestingly, Pipp et al. [14] demonstrated the importance of FSS in arteriogenesis by means of a porcine ischemic hindlimb model with extremely high levels of collateral flow and FSS. Normally, during the later phases of arteriogenesis, FSS decreases as the collateral diameter increases so that FSS normalizes. This drop in FSS acts as a signal to arrest proliferation and as a result, prevents further collateral growth before an optimal adaptation

[Seite 1381]

is reached. Pipp and colleagues [14] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further, significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic power in collateral growth.


14. Pipp, F., Boehm, S., Cai, W. J., Adili, F., Ziegler, B., Karanovic, G., Ritter, R., Balzer, J., Scheler, C., Schaper, W., Schmitz-Rixen, T. (2004) Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. Arterioscler. Thromb. Vasc. Biol. 24, 1664–1668.

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[Studying vascular development or the mechanisms of neovascularisation (angiogenesis, arteriogenesis or vasculogenesis) and evaluating the effects of pro or antiangiogenic] strategies require complete and accurate analysis of the neoformed vascular network. However, methods of assessment, such as histology with confocal or two-photon microscopy, laser Doppler, microangiography, fluorescent microspheres, magnetic resonance angiography, positron emission tomography, are not always precise or quantitative; they focus on a limited area of study, reveal capillary density primarily in 2 dimensions, and represent superficial blood flow[137].

137. Couffinhal, T., et al., Mouse model of angiogenesis. Am J Pathol, 1998. 152(6): p. 1667-79.

Studying vascular development or the mechanisms of neovascularisation (angiogenesis, arteriogenesis or vasculogenesis) and evaluating the effects of pro or antiangiogenic strategies require complete and accurate analysis of the neoformed vascular network. However, methods of assessment, such as histology with confocal or two-photon microscopy, laser Doppler, microangiography, fluorescent microspheres, magnetic resonance angiography, positron emission tomography, are not always precise or quantitative; they focus on a limited area of study, reveal capillary density primarily in 2 dimensions, and represent superficial blood flow (for details see review [1]).

1. Couffinhal T, Dufourcq P, Barandon L, Leroux L, Duplaa C: Mouse models to study angiogenesis in the context of cardiovascular diseases. Front Biosci 2009, 14:3310-3325.

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Surgical ligation of the femoral artery at a specific site triggers arteriogenesis of small, pre-existing collateral arteries into functional conduit vessels proximally and ischemic angiogenesis distally. The vascular response to hind-limb ischemia can be readily evaluated by laser Doppler-based perfusion measurements, histological quantification of arteriogenesis and MicroCT imaging. Surgical ligation of the femoral artery at a specific site triggers arteriogenesis of small, pre-existing collateral arteries into functional conduit vessels proximally and ischemic angiogenesis distally. The vascular response to hind-limb ischemia can be readily evaluated by laser Doppler-based perfusion measurements, histological quantification of arteriogenesis and angiogenesis or whole-mount visualization of arteries in limb muscles.
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Gap junctions play a multifaceted role in the vasculature that is essential in the control of gene expression, vascular development, and vascular function. However, the function of gap junctions in the vasculature does not depend only on the molecular selectivity or permeability of the different vascular connexin isoforms. [...] Although the participation of the gap junction in vascular function seems to be very complex, the development of connexin-knockout animals has been a great contribution to our understanding of how these proteins work in the vasculature.

In addition, connexin-mimetic peptides have been demonstrated to be an effective tool to dissect the participation of gap junctions in vascular function.

Gap junctions play a multifaceted role in the vasculature that is essential in the control of gene expression, vascular development, and vascular function. However, the function of gap junctions in the vasculature does not depend only on the molecular selectivity or permeability of the different vascular connexin isoforms.

[Seite 260]

Although the participation of the gap junction in vascular function seems to be very complex, the development of connexin-knockout animals has been a great contribution to our understanding of how these proteins work in the vasculature. In addition, connexin-mimetic peptides have demonstrated to be an effective tool to dissect the participation of gap junctions in vascular function.

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Arteriogenesis (collateral vessel growth) is triggered by fluid shear stress in case of an arterial occlusion. It is an important focus in current cardiovascular research as it might provide new therapeutic opportunities. But the molecular mechanisms underlying arteriogenesis are not yet completely understood. Arteriogenesis (collateral vessel growth) is triggered by fluid shear stress in case of an arterial occlusion. It is an important focus in current cardiovascular research as it might provide new therapeutic opportunities. Although the molecular mechanisms underlying arteriogenesis are not yet completely understood, it has been shown that monocytes/macrophages and lymphocytes, in particular NK- and Tlymphocytes, play an important role in arteriogenesis.
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Connexin 37 and Connexin 40 (Cx37, Cx40) are the major gap junction proteins expressed in vascular endothelial cells[85-89]. These proteins are very dynamic, exhibiting rapid turnover times and variable expression patterns. Although the extent of combinations of different connexins within connexons and channels remains unclear, immunohistochemical and immunocytochemical studies demonstrate differential expression and localization patterns of both vascular connexins in endothelium, depending on species[97], vascular bed[98-100], and local hemodynamics[101].[...] For the microcirculation in vivo studies implicate Cx40 as the constitutive vascular gap junction protein across species [and vascular bed, playing an important role in coupling between cells in the vascular wall[78, 97-98], particularly in response to changes in tissue metabolic demand.]

78. de Wit, C., et al., Impaired conduction of vasodilation along arterioles in connexin40-deficient mice. Circ Res, 2000. 86(6): p. 649-55.

85. Bruzzone, R., et al., Connexin40, a component of gap junctions in vascular endothelium, is restricted in its ability to interact with other connexins. Mol Biol Cell, 1993. 4(1): p. 7-20.

86. Larson, D.M., C.C. Haudenschild, and E.C. Beyer, Gap junction messenger RNA expression by vascular wall cells. Circ Res, 1990. 66(4): p. 1074-80.

87. Little, T.L., E.C. Beyer, and B.R. Duling, Connexin 43 and connexin 40 gap junctional proteins are present in arteriolar smooth muscle and endothelium in vivo. Am J Physiol, 1995. 268(2 Pt 2): p. H729-39.

88. Reed, K.E., et al., Molecular cloning and functional expression of human connexin37, an endothelial cell gap junction protein. J Clin Invest, 1993. 91(3): p. 997-1004.

89. Van Rijen, H., et al., Gap junctions in human umbilical cord endothelial cells contain multiple connexins. Am J Physiol, 1997. 272(1 Pt 1): p. C117-30.

97. van Kempen, M.J. and H.J. Jongsma, Distribution of connexin37, connexin40 and connexin43 in the aorta and coronary artery of several mammals. Histochem Cell Biol, 1999. 112(6): p. 479-86. 98. Hill, C.E., et al., Heterogeneity in the distribution of vascular gap junctions and connexins: implications for function. Clin Exp Pharmacol Physiol, 2002. 29(7): p. 620-5.

99. Pepper, M.S., et al., Coupling and connexin 43 expression in microvascular and large vessel endothelial cells. Am J Physiol, 1992. 262(5 Pt 1): p. C1246-57.

100. Yeh, H.I., et al., Individual gap junction plaques contain multiple connexins in arterial endothelium. Circ Res, 1998. 83(12): p. 1248-63.

101. Gabriels, J.E. and D.L. Paul, Connexin43 is highly localized to sites of disturbed flow in rat aortic endothelium but connexin37 and connexin40 are more uniformly distributed. Circ Res, 1998. 83(6): p. 636-43.

Connexin 37, 40, and 43 (Cx37, Cx40, Cx43, respectively) are the major gap junction proteins expressed in vascular endothelial cells (7, 32, 34, 39, 45). These proteins are very dynamic, exhibiting rapid turnover times and variable expression patterns. [...]

Although the extent of combinations of different connexins within connexons and channels remains unclear, immunohistochemical and immunocytochemical studies demonstrate differential expression and localization patterns of all three vascular connexins in endothelium, depending on species (44), vascular bed (25, 37, 53), and local hemodynamics (21). In vivo studies implicate Cx40 as the constitutive vascular gap junction protein across species and vascular bed, playing an important role in coupling between cells in the vascular wall (44).


7. Bruzzone R, Haefliger JA, Gimlich RL, and Paul DL. Connexin40, a component of gap junctions in vascular endothelium, is restricted in its ability to interact with other connexins. Mol Biol Cell 4: 7–20, 1993.

21. Gabriels JE and Paul DL. Connexin43 is highly localized to sites of disturbed flow in rat aortic endothelium but connexin37 and connexin40 are more uniformly distributed. Circ Res 83: 636–643, 1998.

25. Hill CE, Rummery N, Hickey H, and Sandow SL. Heterogeneity in the distribution of vascular gap junctions and connexins: implications for function. Clin Exp Pharmacol Physiol 29: 620–625, 2002.

32. Larson DM, Haudenschild CC, and Beyer EC. Gap junction messenger RNA expression by vascular wall cells. Circ Res 66: 1074–1080, 1990.

34. Little TL, Beyer EC, and Duling BR. Connexin 43 and connexin 40 gap junctional proteins are present in arteriolar smooth muscle and endothelium in vivo. Am J Physiol Heart Circ Physiol 268: H729–H739, 1995.

37. Pepper MS, Montesano R, el Aoumari A, Gros D, Orci L, and Meda P. Coupling and connexin 43 expression in microvascular and large vessel endothelial cells. Am J Physiol Cell Physiol 262: C1246–C1257, 1992.

39. Reed KE, Westphale EM, Larson DM, Wang HZ, Veenstra RD, and Beyer EC. Molecular cloning and functional expression of human connexin37, an endothelial cell gap junction protein. J Clin Invest 91: 997–1004, 1993.

44. Van Kempen MJ and Jongsma HJ. Distribution of connexin37, connexin40 and connexin43 in the aorta and coronary artery of several mammals. Histochem Cell Biol 112: 479–486, 1999.

45. Van Rijen H, van Kempen MJ, Analbers LJ, Rook MB, van Ginneken AC, Gros D, and Jongsma HJ. Gap junctions in human umbilical cord endothelial cells contain multiple connexins. Am J Physiol Cell Physiol 272: C117–C130, 1997.

53. Yeh HI, Rothery S, Dupont E, Coppen SR, and Severs NJ. Individual gap junction plaques contain multiple connexins in arterial endothelium. Circ Res 83: 1248–1263, 1998.

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Gap junctions are essential for many physiological processes, such as the coordinated depolarization of cardiac muscle, and proper embryonic development. [...] For this reason, mutations in connexin-encoding genes can lead to functional and developmental abnormalities. Gap junctions are essential for many physiological processes, such as the coordinated depolarization of cardiac muscle, and proper embryonic development. For this reason, mutations in connexin-encoding genes can lead to functional and developmental abnormalities.
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[Although the extent of combinations of different connexins within connexons and] channels remains unclear, immunohistochemical and immunocytochemical studies demonstrate differential expression and localization patterns of all three vascular connexins in the endothelium, depending on species[97], vascular bed[98-100], and local hemodynamics[101]. In vivo studies implicate Cx40 as the constitutive vascular gap junction protein across species and vascular bed, playing an important role in coupling between cells in the vascular wall[97].

97. van Kempen, M.J. and H.J. Jongsma, Distribution of connexin37, connexin40 and connexin43 in the aorta and coronary artery of several mammals. Histochem Cell Biol, 1999. 112(6): p. 479-86.

98. Hill, C.E., et al., Heterogeneity in the distribution of vascular gap junctions and connexins: implications for function. Clin Exp Pharmacol Physiol, 2002. 29(7): p. 620-5.

99. Pepper, M.S., et al., Coupling and connexin 43 expression in microvascular and large vessel endothelial cells. Am J Physiol, 1992. 262(5 Pt 1): p. C1246-57.

100. Yeh, H.I., et al., Individual gap junction plaques contain multiple connexins in arterial endothelium. Circ Res, 1998. 83(12): p. 1248-63.

101. Gabriels, J.E. and D.L. Paul, Connexin43 is highly localized to sites of disturbed flow in rat aortic endothelium but connexin37 and connexin40 are more uniformly distributed. Circ Res, 1998. 83(6): p. 636-43.

Although the extent of combinations of different connexins within connexons and channels remains unclear, immunohistochemical and immunocytochemical studies demonstrate differential expression and localization patterns of all three vascular connexins in endothelium, depending on species (44), vascular bed (25, 37, 53), and local hemodynamics (21). In vivo studies implicate Cx40 as the constitutive vascular gap junction protein across species and vascular bed, playing an important role in coupling between cells in the vascular wall (44).

21. Gabriels JE and Paul DL. Connexin43 is highly localized to sites of disturbed flow in rat aortic endothelium but connexin37 and connexin40 are more uniformly distributed. Circ Res 83: 636–643, 1998.

25. Hill CE, Rummery N, Hickey H, and Sandow SL. Heterogeneity in the distribution of vascular gap junctions and connexins: implications for function. Clin Exp Pharmacol Physiol 29: 620–625, 2002.

37. Pepper MS, Montesano R, el Aoumari A, Gros D, Orci L, and Meda P. Coupling and connexin 43 expression in microvascular and large vessel endothelial cells. Am J Physiol Cell Physiol 262: C1246–C1257, 1992.

44. Van Kempen MJ and Jongsma HJ. Distribution of connexin37, connexin40 and connexin43 in the aorta and coronary artery of several mammals. Histochem Cell Biol 112: 479–486, 1999.

53. Yeh HI, Rothery S, Dupont E, Coppen SR, and Severs NJ. Individual gap junction plaques contain multiple connexins in arterial endothelium. Circ Res 83: 1248–1263, 1998.

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Connexins 37, 40, and 43 (Cx37, Cx40, Cx43, respectively) are the major gap junction proteins expressed in vascular endothelial cells[85-89]. These proteins are very dynamic, exhibiting rapid turnover times and variable expression patterns. Because of the unique gating and permselective characteristics of Cx37, Cx40, and Cx43, different combinations of these connexin isoforms contribute to homo- or heteromeric connexons and homo- or heterotypic gap junctions leading to a variety of channel types with different functional properties[83, 90-96].

83. Kumar, N.M. and N.B. Gilula, The gap junction communication channel. Cell, 1996. 84(3): p. 381-8.

85. Bruzzone, R., et al., Connexin40, a component of gap junctions in vascular endothelium, is restricted in its ability to interact with other connexins. Mol Biol Cell, 1993. 4(1): p. 7-20.

86. Larson, D.M., C.C. Haudenschild, and E.C. Beyer, Gap junction messenger RNA expression by vascular wall cells. Circ Res, 1990. 66(4): p. 1074-80.

87. Little, T.L., E.C. Beyer, and B.R. Duling, Connexin 43 and connexin 40 gap junctional proteins are present in arteriolar smooth muscle and endothelium in vivo. Am J Physiol, 1995. 268(2 Pt 2): p. H729-39.

88. Reed, K.E., et al., Molecular cloning and functional expression of human connexin37, an endothelial cell gap junction protein. J Clin Invest, 1993. 91(3): p. 997-1004.

89. Van Rijen, H., et al., Gap junctions in human umbilical cord endothelial cells contain multiple connexins. Am J Physiol, 1997. 272(1 Pt 1): p. C117-30.

90. Beblo, D.A. and R.D. Veenstra, Monovalent cation permeation through the connexin40 gap junction channel. Cs, Rb, K, Na, Li, TEA, TMA, TBA, and effects of anions Br, Cl, F, acetate, aspartate, glutamate, and NO3. J Gen Physiol, 1997. 109(4): p. 509-22.

91. Bruzzone, R., T.W. White, and D.A. Goodenough, The cellular Internet: on-line with connexins. Bioessays, 1996. 18(9): p. 709-18.

92. Bruzzone, R., T.W. White, and D.L. Paul, Connections with connexins: the molecular basis of direct intercellular signaling. Eur J Biochem, 1996. 238(1): p. 1-27.

93. Elfgang, C., et al., Specific permeability and selective formation of gap junction channels in connexin-transfected HeLa cells. J Cell Biol, 1995. 129(3): p. 805-17.

94. Veenstra, R.D., Size and selectivity of gap junction channels formed from different connexins. J Bioenerg Biomembr, 1996. 28(4): p. 327-37.

95. Wang, H.Z. and R.D. Veenstra, Monovalent ion selectivity sequences of the rat connexin43 gap junction channel. J Gen Physiol, 1997. 109(4): p. 491-507.

96. White, T.W. and R. Bruzzone, Multiple connexin proteins in single intercellular channels: connexin compatibility and functional consequences. J Bioenerg Biomembr, 1996. 28(4): p. 339-50.

Connexin 37, 40, and 43 (Cx37, Cx40, Cx43, respectively) are the major gap junction proteins expressed in vascular endothelial cells (7, 32, 34, 39, 45). These proteins are very dynamic, exhibiting rapid turnover times and variable expression patterns. Because of the unique gating and permselective characteristics of Cx37, Cx40, and Cx43, different combinations of these connexin isoforms contribute to homo- or heteromeric connexons and homo- or heterotypic gap junctions leading to a variety of channel types with different functional properties (1, 8, 9, 19, 28, 47–49).

1. Beblo DA and Veenstra RD. Monovalent cation permeation through the connexin40 gap junction channel: Cs, Rb, K, Na, Li, TEA, TMA, TBA, and effects of anions Br, Cl, F, acetate, aspartate, glutamate, and NO3. J Gen Physiol 109: 509–522, 1997.

7. Bruzzone R, Haefliger JA, Gimlich RL, and Paul DL. Connexin40, a component of gap junctions in vascular endothelium, is restricted in its ability to interact with other connexins. Mol Biol Cell 4: 7–20, 1993.

8. Bruzzone R, White TW, and Goodenough DA. The cellular internet: on-line with connexins. Bioessays 18: 709–718, 1996.

9. Bruzzone R, White TW, and Paul DL. Connections with connexins: the molecular basis of direct intercellular signaling. Eur J Biochem 238: 1–27, 1996.

19. Elfgang C, Eckert R, Lichtenberg-Frate´ H, Butterweck A, Traub O, Klein TA, Hüsler DF, and Willecke K. Specific permeability and selective formation of gap junction channels in connexin-transfected HeLa cells. J Cell Biol 129: 805–817, 1995.

28. Kumar NM and Gilula NB. The gap junction communication channel. Cell 84: 381–388, 1996.

29. Kwak BR and Jongsma HJ. Selective inhibition of gap junction channel activity by synthetic peptides. J Physiol 516: 679–685, 1999.

32. Larson DM, Haudenschild CC, and Beyer EC. Gap junction messenger RNA expression by vascular wall cells. Circ Res 66: 1074–1080, 1990.

34. Little TL, Beyer EC, and Duling BR. Connexin 43 and connexin 40 gap junctional proteins are present in arteriolar smooth muscle and endothelium in vivo. Am J Physiol Heart Circ Physiol 268: H729–H739, 1995.

39. Reed KE, Westphale EM, Larson DM, Wang HZ, Veenstra RD, and Beyer EC. Molecular cloning and functional expression of human connexin37, an endothelial cell gap junction protein. J Clin Invest 91: 997–1004, 1993.

45. Van Rijen H, van Kempen MJ, Analbers LJ, Rook MB, van Ginneken AC, Gros D, and Jongsma HJ. Gap junctions in human umbilical cord endothelial cells contain multiple connexins. Am J Physiol Cell Physiol 272: C117–C130, 1997.

47. Veenstra RD. Size and selectivity of gap junction channels formed from different connexins. J Bioenerg Biomembr 28:b 327–337, 1996.

48. Wang HZ and Veenstra RD. Monovalent ion selectivity sequences of the rat connexin43 gap junction channel. J Gen Physiol 109: 491–507, 1997.

49. White TW and Bruzzone R. Multiple connexin proteins in single intercellular channels: connexin compatibility and functional consequences. J Bioenerg Biomembr 28: 339–350, 1996.

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Endothelial gap junctions are channels that permit and strictly regulate communication throughout the endothelial monolayer and between endothelial cells and adjacent smooth muscle and circulating blood cells. Endothelial cell migration and growth, particularly following injury and during angiogenesis, depend on communication through gap junctions[71-75]. In addition, gap junctions coordinate vascular tone and vasomotion [76-78] and participate in the regulation of immunoinflammatory responses[79, 80].

[...] Gap junctions are formed by a pair of hemichannels called connexons, each contributed by one of two neighboring cells. Connexons are composed of six connexin monomer subunits arranged around a central pore(Fig.1.6.)[82].


71. Kwak, B.R., et al., Inhibition of endothelial wound repair by dominant negative connexin inhibitors. Mol Biol Cell, 2001. 12(4): p. 831-45.

72. Larson, D.M., et al., Differential regulation of connexin43 and connexin37 in endothelial cells by cell density, growth, and TGF-beta1. Am J Physiol, 1997. 272(2 Pt 1): p. C405-15.

73. Pepper, M.S., et al., Junctional communication is induced in migrating capillary endothelial cells. J Cell Biol, 1989. 109(6 Pt 1): p. 3027-38.

74. Xie, H.Q. and V.W. Hu, Modulation of gap junctions in senescent endothelial cells. Exp Cell Res, 1994. 214(1): p. 172-6.

75. Yeh, H.I., et al., Age-related alteration of gap junction distribution and connexin expression in rat aortic endothelium. J Histochem Cytochem, 2000. 48(10): p. 1377-89.

76. Chaytor, A.T., W.H. Evans, and T.M. Griffith, Central role of heterocellular gap junctional communication in endothelium-dependent relaxations of rabbit arteries. J Physiol, 1998. 508 ( Pt 2): p. 561-73.

77. Christ, G.J., et al., Gap junctions in vascular tissues. Evaluating the role of intercellular communication in the modulation of vasomotor tone. Circ Res, 1996. 79(4): p. 631-46.

78. de Wit, C., et al., Impaired conduction of vasodilation along arterioles in connexin40-deficient mice. Circ Res, 2000. 86(6): p. 649-55.

79. Oviedo-Orta, E., R.J. Errington, and W.H. Evans, Gap junction intercellular communication during lymphocyte transendothelial migration. Cell Biol Int, 2002. 26(3): p. 253-63.

80. Wong, C.W., T. Christen, and B.R. Kwak, Connexins in leukocytes: shuttling messages? Cardiovasc Res, 2004. 62(2): p. 357-67.

82. Sohl, G. and K. Willecke, Gap junctions and the connexin protein family. Cardiovasc Res, 2004. 62(2): p. 228-32.

Endothelial gap junctions are channels that permit and strictly regulate communication throughout the endothelial monolayer and between endothelial cells and adjacent smooth muscle and circulating blood cells. Endothelial cell migration and growth, particularly following injury and during angiogenesis, depend on communication through gap junctions (31, 33, 38, 51, 52). In addition, gap junctions coordinate vascular tone and vasomotion (11, 13, 17) and participate in the regulation of immunoinflammatory responses (36, 50).

Gap junctions are formed by a pair of hemichannels called connexons, each contributed by one of two neighboring cells. Connexons are composed of six connexin monomer subunits arranged around a central pore.


11. Chaytor AT, Evans WH, and Griffith TM. Central role of heterocellular gap junctional communication in endothelium-dependent relaxations of rabbit arteries. J Physiol 508: 561–573, 1998.

13. Christ GJ, Spray DC, el-Sabban M, Moore LK, and Brink PR. Gap junctions in vascular tissues. Evaluating the role of intercellular communication in the modulation of vasomotor tone. Circ Res 79: 631–646, 1996.

17. De Wit C, Roos F, Bolz SS, Kirchhoff S, Krüger O, Willecke K, and Pohl U. Impaired conduction of vasodilation along arterioles in connexin40-deficient mice. Circ Res 86: 649–655, 2000.

31. Kwak BR, Pepper MS, Gros DB, and Meda P. Inhibition of endothelial wound repair by dominant negative connexin inhibitors. Mol Biol Cell 12: 831–845, 2001.

33. Larson DM, Wrobleski MJ, Sagar GD, Westphale EM, and Beyer EC. Differential regulation of connexin43 and connexin37 in endothelial cells by cell density, growth, and TGF-beta1. Am J Physiol Cell Physiol 272: C405–C415, 1997.

36. Oviedo-Orta E, Errington RJ, and Evans WH. Gap junction intercellular communication during lymphocyte transendothelial migration. Cell Biol Int 26: 253–263, 2002.

38. Pepper MS, Spray DC, Chanson M, Montesano R, Orci L, and Meda P. Junctional communication is induced in migrating capillary endothelial cells. J Cell Biol 109: 3027–3038, 1989.

50. Wong CW, Christen T, and Kwak BR. Connexins in leukocytes: shuttling messages? Cardiovasc Res 62: 357–367, 2004.

51. Xie HQ and Hu VW. Modulation of gap junctions in senescent endothelial cells. Exp Cell Res 214: 172–176, 1994.

52. Yeh HI, Chang HM, Lu WW, Lee YN, Ko YS, Severs NJ, and Tsai CH. Age-related alteration of gap junction distribution and connexin expression in rat aortic endothelium. J Histochem Cytochem 48: 1377–1389, 2000.

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[45.] Haw/Fragment 016 19 - Diskussion
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Connexins are four-pass transmembrane proteins with both C and N cytoplasmic termini, a cytoplasmic loop (CL) and two extra-cellular loops, (EL-1) and (EL-2). Connexins are assembled in groups of six to form hemichannels, or connexons, and two hemichannels then combine to form a gap junction. They usually weigh between 26 and 60 kDa, and have an average length of 380 amino acids. The various connexins have been observed to combine into both homomeric and heteromeric gap junctions, each of which may exhibit different functional properties including pore conductance, size selectivity, charge selectivity, voltage gating, and chemical gating. Connexins are four-pass transmembrane proteins with both C and N cytoplasmic termini, a cytoplasmic loop (CL) and two extra-cellular loops, (EL-1) and (EL-2). Connexins are assembled in groups of six to form hemichannels, or connexons, and two hemichannels then combine to form a gap junction. [...] They usually weigh between 26 and 60 kDa, and have an average length of 380 amino acids. The various connexins have been observed to combine into both homomeric and heteromeric gap junctions, each of which may exhibit different functional properties including pore conductance, size selectivity, charge selectivity, voltage gating, and chemical gating.
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Connexins, or gap junction proteins, are a family of structurally-related transmembrane proteins that assemble to form vertebrate gap junctions (an entirely different family of proteins, the innexins, form gap junctions in invertebrates)[81].

81. Lodish, H.F., R.K. Rodriguez, and D.J. Klionsky, Points of view: lectures: can't learn with them, can't learn without them. Cell Biol Educ, 2004. 3(4): p. 202-11.

Connexins, or gap junction proteins, are a family of structurally-related transmembrane proteins that assemble to form vertebrate gap junctions (an entirely different family of proteins, the innexins, form gap junctions in invertebrates).[1]

1. Lodish, Harvey F.; Arnold Berk, Paul Matsudaira, Chris A. Kaiser, Monty Krieger, Mathew P. Scott, S. Lawrence Zipursky, James Darnell (2004). Molecular Cell Biology (5th ed.). New York: W.H. Freeman and Company. pp. 230–1. ISBN 0-7167-4366-3.

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Intercellular communication is a key regulator of vascular function[69, 70]. In the vessel wall, cell-to-cell communication occurs by extracellular diffusion and convection of humoral factors or by intercytoplasmic exchange of ions, metabolites, [and small signaling molecules (<1 kDa) via gap junctions.]

69. Haefliger, J.A., P. Nicod, and P. Meda, Contribution of connexins to the function of the vascular wall. Cardiovasc Res, 2004. 62(2): p. 345-56.

70. Ross, R., Cell biology of atherosclerosis. Annu Rev Physiol, 1995. 57: p. 791-804.

INTERCELLULAR COMMUNICATION is a key regulator of vascular function (23, 40). In the vessel wall, cell-to-cell communication occurs by extracellular diffusion and convection of humoral factors or by intercytoplasmic exchange of ions, metabolites, and small signaling molecules (<1 kDa) via gap junctions.

23. Haefliger JA, Nicod P, and Meda P. Contribution of connexins to the function of the vascular wall. Cardiovasc Res 62: 345–356, 2004.

40. Ross R. Cell biology of atherosclerosis. Annu Rev Physiol 57: 791–804, 1995.

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[The same results can be obtained with] intravenous infusion of anti–ICAM-1 antibodies that also prevent monocyte attachment. Targeted disruption of the MCP-1 receptor (CC chemokines receptor-2) (CCR-2) in mice prevented almost all collateral growth after femoral artery occlusion[59], but infusion of MCP-1 into the proximal stump of the occluded femoral artery led to increased monocyte influx and elicited a strong arteriogenic effect[60]. We also discovered that the weak arteriogenic effects of chronically infused vascular endothelial growth factor-A (VEGF-A) is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes[61]. A similar effect was discovered with placenta growth factor (PlGF). The arteriogenesis-inhibiting effect of targeted disruption of PlGF in mice [62] could be lifted by bone marrow transplantation, i.e., an effect of monocytes[62, 63]. Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation[64]. Intravenous infusion of liposome-packaged phosphonates (alendronate) destroyed all monocytes/macrophages for a period of ≈1 week. During this time, VEGF and PlGF infusions remained completely inactive, showing again the importance of monocytes in arteriogenesis[64]. Suppression of monocyte counts by treatment with 5-fluorouracil (5-FU) significantly delayed arteriogenesis, but the rebound effect after chemical bone marrow suppression had the opposite effect[20, 59].

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

59. Heil, M., et al., Blood monocyte concentration is critical for enhancement of collateral artery growth. Am J Physiol Heart Circ Physiol, 2002. 283(6): p. H2411-9.

60. Ito, W.D., et al., Monocyte chemotactic protein-1 increases collateral and peripheral conductance after femoral artery occlusion. Circ Res, 1997. 80(6): p. 829-37.

61. Breier, G., et al., Transforming growth factor-beta and Ras regulate the VEGF/VEGF-receptor system during tumor angiogenesis. Int J Cancer, 2002. 97(2): p. 142-8.

62. Carmeliet, P., et al., Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions. Nat Med, 2001. 7(5): p. 575-83.

63. Scholz, D., et al., Bone marrow transplantation abolishes inhibition of arteriogenesis in placenta growth factor (PlGF) -/- mice. J Mol Cell Cardiol, 2003. 35(2): p. 177-84.

64. Pipp, F., et al., VEGFR-1-selective VEGF homologue PlGF is arteriogenic: evidence for a monocyte-mediated mechanism. Circ Res, 2003. 92(4): p. 378-85.

The same results can be obtained with intravenous infusion of anti–ICAM-1 antibodies that also prevent monocyte attachment. Targeted disruption of the MPC-1 receptor (CCR-2) in mice prevents almost all collateral growth after femoral artery occlusion,43 but infusion of MCP-1 into the proximal stump of the occluded femoral artery led to increased monocyte influx and elicited a strong arteriogenic effect.44 We also discovered that the weak arteriogenic effects of chronically infused VEGF A is caused by the monocyte attractant effect of VEGF that binds to the VEGF receptor 1, which is exclusively present on monocytes.45 A similar effect was discovered with placenta growth factor (PlGF). The arteriogenesis-inhibiting effect of targeted disruption of PlGF in mice46 could be lifted by bone marrow transplantation, ie, an effect of monocytes.46,47 Because infusion of VEGF-E, which binds exclusively to VEGFR-2, did not influence arteriogenesis, we concluded that the effects of VEGF-A on arteriogenesis are caused by monocyte activation.48 Intravenous infusion of liposome-packaged phosphonates (alendronate) destroyed all monocytes/macrophages for a period of ≈1 week. During this time, VEGF and PlGF infusions remained completely inactive, showing again the importance of monocytes in arteriogenesis.48

Suppression of monocyte counts by treatment with 5-fluorouracil significantly delayed arteriogenesis, but the rebound effect after chemical bone marrow suppression had the opposite effect.49


43. Heil M, Ziegelhoeffer T, Helisch A, Wagner S, Martin S, Kuziel WA, Schaper W. Arteriogenesis (collateral artery growth) after femoral artery occlusion is reduced in mice lacking CC-chemokine-receptor-2. Circulation. 2002;106 (Suppl II):1390. Abstract.

44. Ito W, Arras M, Winkler B, Scholz D, Schaper J, Schaper W. Monocyte chemotactic protein-1 increases collateral and peripheral conductance after femoral artery occlusion. Circ Res. 1997;80:829–837.

45. Breier G, Blum S, Peli J, Groot M, Wild C, Risau W, Reichmann E. Transforming growth factor-b1 and Ras regulate the VEGF/VEGF receptor system during tumor angiogenesis. Int J Cancer. 2002;97: 142–148.

46. Carmeliet P, Moons L, Luttun A, Vincenti V, Compernolle V, De Mol M, Wu Y, Bono F, Devy L, Beck H, Scholz D, Acker T, DiPalma T, Dewerchin M, Noel A, Stalmans I, Barra A, Blacher S, Vandendriessche T, Ponten A, Eriksson U, Plate K, Foidart J-M, Schaper W, Charnock-Jones DS, Hicklin DJ, Herbert J-M, Collen D, Persico G. Synergism between vascular endothelial growth factor and placental growth factor contributes to angiogenesis and plasma extravasation in pathological conditions. Nature Med. 2001;7:575–583.

47. Scholz D, Elsaesser H, Sauer A, Friedrich C, Luttun A, Carmeliet P, Schaper W. Bone marrow transplantation abolishes inhibition of arteriogenesis in placenta growth factor (PlGF) -/- mice. J Mol Cell Cardiol. 2003;35:177–184.

48. Pipp F, Heil M, Issbrücker K, Ziegelhöffer T, Martin S, van den Heuvel J, Weich H, Fernandez B, Clauss M, Schaper W. VEGFR-1-selective VEGF homologue PlGF is arteriogenic: evidence for a monocytemediated mechanism. Circ Res. 2003;92:378–385.

49. Heil M, Ziegelhoeffer T, Pipp F, Kostin S, Martin S, Clauss M, Schaper W. Blood monocytes concentration is critical for enhancement of collateral artery growth. Am J Physiol Heart Circ Physiol. 2002;283: H2411–H2419.

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The endothelial lining of growing canine coronary collaterals is studded with monocytes that had attached, during phase 1 of arteriogenesis, to the now much rougher surface of the swollen endothelial cells that, activated by shear stress, upregulate the MCP-1 and adhesion molecules to which the macrophage 1 antigen (Mac-1) receptor of monocytes binds[55]. Infusion of soluble ICAM-1 binds to circulating monocytes and prevents their adhesion to transforming arterioles.

55. Scholz, D., et al., Ultrastructure and molecular histology of rabbit hind-limb collateral artery growth (arteriogenesis). Virchows Arch, 2000. 436(3): p. 257-70.

The endothelial lining of growing canine coronary collaterals is studded with monocytes that had attached, during phase 1 of arteriogenesis, to the now much rougher surface of the swollen endothelial cells that, activated by shear stress, upregulate the monocyte chemoattractant MCP-1 and adhesion molecules11 to which the Mac-1 receptor of monocytes binds. Infusion of soluble ICAM-1 binds to circulating monocytes and prevents their adhesion to transforming arterioles.

11. Scholz D, Ito W, Fleming I, Deindl E, Sauer A, Babiak A, Bühler A, Wiesnet M, Busse R, Schaper J, Schaper W. Ultrastructure and molecular histology of rabbit hindlimb collateral artery growth. Virchows Arch. 2000;436:257–270.

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[The location and nature of the mechanotransducer of shear stress are controversially] discussed[53], and protein kinases and stretch sensitive K-channels were studied[54]. We found that high shear stress in vitro causes a transient phosphorylation of focal adhesions, which could also act as mechanoreceptors[55]. By whatever way the mechanical force is transmitted from the deformed cell (membrane) to its nucleus, it will activate transcription factors, like early growth response 1 (egr-1) (upregulated during the early phases of arteriogenesis), that switch on gene expression, notably of chemokines like MCP-1 but also adhesion molecules like intracellular adhesion molecule-1 (ICAM-1), that are necessary for the docking of monocytes[56]. Shear stress is also known to release NO, but it is not known whether chronically increased shear stress will lead to chronically increased amounts of released NO. A lasting steep increase in shear stress leads only to a transient increase of egr-1, and this may also happen with the NO response[57]. The increased permeability of immature collaterals may have been caused by NO. However, expression studies on the RNA level have not shown any changes related to the early stages of collateral growth[20]. Immunofluorescence studies have shown the presence of PDGF antigen in neointima formation in canine collaterals, which supports findings by the Geary,R.L., et al[58]. showing that PDGF is increased under low-flow conditions that favor intima proliferation. The necessity of a cell-to cell transmitter (i.e., from endothelium to smooth muscle) is not very high, because the adhering monocyte assumes that function.

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

53. Ali, M.H. and P.T. Schumacker, Endothelial responses to mechanical stress: where is the mechanosensor? Crit Care Med, 2002. 30(5 Suppl): p. S198-206.

54. Nilius, B. and G. Droogmans, Ion channels and their functional role in vascular endothelium. Physiol Rev, 2001. 81(4): p. 1415-59.

55. Scholz, D., et al., Ultrastructure and molecular histology of rabbit hind-limb collateral artery growth (arteriogenesis). Virchows Arch, 2000. 436(3): p. 257-70.

56. Gimbrone, M.A., Jr., et al., Hemodynamics, endothelial gene expression, and atherogenesis. Ann N Y Acad Sci, 1997. 811: p. 1-10; discussion 10-1.

57. Khachigian, L.M., et al., Egr-1 is activated in endothelial cells exposed to fluid shear stress and interacts with a novel shear-stress-response element in the PDGF A-chain promoter. Arterioscler Thromb Vasc Biol, 1997. 17(10): p. 2280-6.

58. Geary, R.L., et al., Time course of flow-induced smooth muscle cell proliferation and intimal thickening in endothelialized baboon vascular grafts. Circ Res, 1994. 74(1): p. 14-23.

The location and nature of the mechanotransducer of shear stress are controversially discussed,35 and protein kinases and stretch sensitive K+ channels were studied.36 We found that high shear stress in vitro causes a transient phosphorylation of focal adhesions,11 which could also act as mechanoreceptors. By whatever way the mechanical force is transmitted from the deformed cell (membrane) to its nucleus, it will activate transcription factors, like egr-1 (upregulated during the early phases of arteriogenesis), that switch on gene expression, notably of chemokines like MCP-1 but also adhesion molecules like intracellular adhesion molecule-1 (ICAM-1), that are necessary for the docking of monocytes. Other transcription factors that are so far not structurally identified may bind to the GAGACC motif present in the promoter region of several growth factors initiating their expression.37 Shear stress is also known to release NO, but it is not known whether chronically increased shear stress will lead to chronically increased amounts of released NO. A lasting step increase in shear stress leads only to a transient increase of egr-1,38 and this may also happen with the NO response. The increased permeability of immature collaterals may have been caused by NO. [...] However, expression studies on the RNA level have, in our hands, not shown any changes related to the early stages of collateral growth. Immunofluorescence studies have shown the presence of PDGF antigen in neointima formation in canine collaterals,39 which supports findings by the Geary et al40 showing that PDGF is increased under low-flow conditions that favor intima proliferation. The necessity of a cell-to-cell transmitter (ie, from endothelium to smooth muscle) is not very high, because the adhering monocyte assumes that function.

11. Scholz D, Ito W, Fleming I, Deindl E, Sauer A, Babiak A, Bühler A, Wiesnet M, Busse R, Schaper J, Schaper W. Ultrastructure and molecular histology of rabbit hindlimb collateral artery growth. Virchows Arch. 2000;436:257–270.

35. Ali MH, Schumacker PT. Endothelial responses to mechanical stress: where is the mechanosensor? Crit Care Med. 2002;30:S198–S206.

36. Nilius B, Droogmans G. Ion channels and their functional role in vascular endothelium. Physiol Rev. 2001;81:1415–1459.

37. Gimbrone MA Jr, Resnick N, Nagel T, Khachigian LM, Collins T, Topper JN. Hemodynamics, endothelial gene expression, and atherogenesis. Ann N Y Acad Sci. 1997;801:1–10.

38. Khachigian LM, Anderson KR, Halnon NJ, Gimbrone MJ, Resnick N, Collins T. Egr-1 is activated in endothelial cells exposed to fluid shear stress and interacts with a novel shear-stress-response element in the PDGF A-chain promoter. Arterioscler Thromb Vasc Biol. 1997;17: 2280–2286.

39. Vosschulte R. Kollateralwachstum. Einflüsse von Wachstumsfaktoren und Matrixmetalloproteinasen auf die Zellproliferation und Zellmigration. In: Max-Planck-Institut für Physiologische und Klinische Forschung. Abteilung Experimentelle Kardiologie. Giessen: Justus-Liebig-Universität Giessen; 1999:88.

40. Geary RL, Kohler TR, Vergel S, Kirkman TR, Clowes AW. Time course of flow-induced smooth muscle cell proliferation and intimal thickening in endothelialized baboon vascular grafts. Circ Res. 1994;74:14–23.

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Chronically increased shear stress activates endothelium in a morphologically visible way. It loses volume control and swells, because chloride channels change their open probability[52]. Inhibitors of the chloride channel also inhibit arteriogenesis. The location and nature of the mechanotransducer of shear stress are controversially [discussed[53], and protein kinases and stretch sensitive K-channels were studied[54].]

52. Nilius, B., et al., Volume-activated Cl- channels. Gen Pharmacol, 1996. 27(7): p. 1131-40.

53. Ali, M.H. and P.T. Schumacker, Endothelial responses to mechanical stress: where is the mechanosensor? Crit Care Med, 2002. 30(5 Suppl): p. S198-206.

54. Nilius, B. and G. Droogmans, Ion channels and their functional role in vascular endothelium. Physiol Rev, 2001. 81(4): p. 1415-59.

Chronically increased shear stress activates endothelium in a morphologically visible way. It loses volume control and swells,

[Seite 1146]

because chloride channels change their open probability.33 Inhibitors of the chloride channel also inhibit arteriogenesis.34 The location and nature of the mechanotransducer of shear stress are controversially discussed,35 and protein kinases and stretch sensitive K+ channels were studied.36


33. Nilius B, Eggermont J, Voets T, Droogmans G. Volume-activated Cl-channels. Gen Pharmacol. 1996;27:1131–1140.

34. Ziegelhoeffer T, Scholz D, Helish A, Wagner S, Schaper W. Swelling cell-doing well? Volume-regulated chloride channels and arteriogenesis. J Mol Cell Cardiol. 2002;34:A71. Abstract

35. Ali MH, Schumacker PT. Endothelial responses to mechanical stress: where is the mechanosensor? Crit Care Med. 2002;30:S198–S206.

36. Nilius B, Droogmans G. Ion channels and their functional role in vascular endothelium. Physiol Rev. 2001;81:1415–1459.

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[52.] Haw/Fragment 007 09 - Diskussion
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Murray[48] proposed that the vascular system is optimally configured to minimize the amount of mechanical and metabolic work to provide adequate blood flow, and he predicted that FSS is constant throughout the vasculature and that blood flow through each vessel is proportional to that vessel’s diameter cube.

48. Murray, C.D., The Physiological Principle of Minimum Work Applied to the Angle of Branching of Arteries. J Gen Physiol, 1926. 9(6): p. 835-841.

Murray25 proposed that the vascular sytem [sic] is optimally configured to minimize the amount of mechanical and metabolic work to provide adequate blood flow, and he predicted that FSS is constant throughout the vasculature and that blood flow through each vessel is proportional to that vessel’s diameter cube.

25. Murray CD. The physiological principle of minimum work applied to the angle of branching arteries. J Gen Physiol. 1926;9:835–841.

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[53.] Haw/Fragment 007 01 - Diskussion
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[This, together with the premature arrest of arteriogenic growth,] as a result of the drop in FSS in the growing collateral, is a reason that collateral arteries cannot completely compensate the conductance of the artery they have replaced. Initially, during arteriogenesis, several collateral vessels are recruited and proliferate. However, as it is hemodynamically more efficient for fewer, larger arteries to conduct the blood than a greater number of smaller arteries, the smaller vessels regress later on, and those with the higher shear forces continue growing[46].

46. Hoefer, I.E., J.J. Piek, and G. Pasterkamp, Pharmaceutical interventions to influence arteriogenesis: new concepts to treat ischemic heart disease. Curr Med Chem, 2006. 13(9): p. 979-87.

This, together with the premature arrest of arteriogenic growth, as a result of the drop in FSS in the growing collateral, is a reason that collateral arteries cannot completely compensate the conductance of the artery they have replaced. Initially, during arteriogenesis, several collateral vessels are recruited and proliferate. However, as it is hemodynamically more efficient for fewer, larger arteries to conduct the blood than a greater number of smaller arteries, the smaller vessels regress later on, and those with the higher shear forces continue growing [17].

17. Hoefer, I. E., Piek, J. J., Pasterkamp, G. (2006) Pharmaceutical interventions to influence arteriogenesis: new concepts to treat ischemic heart disease. Curr. Med. Chem. 13, 979–987.

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[54.] Haw/Fragment 006 21 - Diskussion
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Furthermore, FSS is almost impossible to measure in small collaterals. Pipp and colleagues[44] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic force in collateral growth.

Collaterals increase their diameter up to 20 times during arteriogenesis, which is possible through mitosis of vascular cells[45]. Given that the collateral vessels grow in length as well as in width, the expanding vessel arranges itself in loops and turns to accommodate the extra length. This gives the vessels a typical corkscrew pattern and causes energy loss[10].


10. Heil, M., et al., Arteriogenesis versus angiogenesis: similarities and differences. J Cell Mol Med, 2006. 10(1): p. 45-55.

44. Pipp, F., et al., Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hindlimb. Arterioscler Thromb Vasc Biol, 2004. 24(9): p. 1664-8.

45. Wolf, C., et al., Vascular remodeling and altered protein expression during growth of coronary collateral arteries. J Mol Cell Cardiol, 1998. 30(11): p. 2291-305.

Furthermore, FSS is almost impossible to measure in small collaterals.

[Seite 1381]

Pipp and colleagues [14] demonstrated that sustained, elevated FSS in their arteriovenous shunt model further, significantly increased the size of collaterals, thus establishing that FSS is a dominant morphogenic power in collateral growth.

Collaterals increase their diameter up to 20 times during arteriogenesis, which is possible through mitosis of vascular cells [15]. Given that the collateral vessels grow in length as well as in width, the expanding vessel arranges itself in loops and turns to accommodate the extra length. This gives the vessels a typical corkscrew pattern [16] and causes energy loss.


14. Pipp, F., Boehm, S., Cai, W. J., Adili, F., Ziegler, B., Karanovic, G., Ritter, R., Balzer, J., Scheler, C., Schaper, W., Schmitz-Rixen, T. (2004) Elevated fluid shear stress enhances postocclusive collateral artery growth and gene expression in the pig hind limb. Arterioscler. Thromb. Vasc. Biol. 24, 1664–1668.

15. Wolf, C., Cai, W. J., Vosschulte, R., Koltai, S., Mousavipour, D., Scholz, D., Afsah-Hedjri, A., Schaper, W., Schaper, J. (1998) Vascular remodeling and altered protein expression during growth of coronary collateral arteries. J. Mol. Cell. Cardiol. 30, 2291–2305.

16. Heil, M., Eitenmuller, I., Schmitz-Rixen, T., Schaper, W. (2006) Arteriogenesis versus angiogenesis: similarities and differences. J. Cell. Mol. Med. 10, 45–55.

Anmerkungen

Ein Verweis auf die Quelle fehlt.

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[55.] Haw/Fragment 006 15 - Diskussion
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FSS is proportional to the blood flow velocity and inversely related to the cube of the radius[41]. It is sensed by the endothelium, which, in response, changes the expression of growth factors, secretes nitric oxide (NO)[42, 43], prostacyclin, and probably other transmitters, and leads, with prolonged exposure, to positive arterial remodeling. However, even small increases in the radius of collateral arteries lead to a precipitous fall of the FSS because of the cubic relationship, and the FSS-related growth ends prematurely[20].

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

41. Schmidt, V.J., et al., Gap junctions synchronize vascular tone within the microcirculation. Pharmacol Rep, 2008. 60(1): p. 68-74.

42. Busse, R. and I. Fleming, Regulation and functional consequences of endothelial nitric oxide formation. Ann Med, 1995. 27(3): p. 331-40.

43. Fleming, I., et al., Isometric contraction induces the Ca2+-independent activation of the endothelial nitric oxide synthase. Proc Natl Acad Sci U S A, 1999. 96(3): p. 1123-8.

FSS is proportional to the blood flow velocity and inversely related to the cube of the radius.21 It is sensed by the endothelium, which, in response, changes the expression of growth factors, secretes NO,22,23 prostacyclin, and probably other transmitters, and leads, with prolonged exposure, to positive arterial remodeling. However, even small increases in the radius of collateral arteries lead to a precipitous fall of the FSS because of the cubic relationship, and the FSS-related growth ends prematurely.

21. Schmidt RF, Thews G. Physiologie des Menschen. Berlin: Springer; 1997.

22. Busse R, Fleming I. Regulation and functional consequences of endothelial nitric oxide formation. Ann Med. 1995;27:331–340.

23. Fleming I, Bauersachs J, Schäfer A, Scholz D, Aldershvile J, Busse R. Isometric contraction induces the Ca2+ independent activation of the endothelial nitric oxide synthase. Proc Natl Acad Sci U S A. 1999;96: 1123–1128.

Anmerkungen

Die Quelle ist in Fn. 20 angegeben. Der Umfang der Übernahme, die drei Literaturverweise miteinschließt, wird aber ebensowenig deutlich wie der Umstand, dass es sich um eine beinahe wörtliche Übernahme handelt.

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(Hindemith), SleepyHollow02

[56.] Haw/Fragment 002 07 - Diskussion
Bearbeitet: 12. October 2014, 16:29 Schumann
Erstellt: 4. October 2014, 17:52 (Hindemith)
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Fig. 1.1.

Haw 02a diss.png

[6] (Van Oostrom, M.C., et al., J Leukoc Biol, 2008;84(6): 1379-91)

Fig.1.1. Neovascularization can occur via vasculogenesis (A), angiogenesis (B), or arteriogenesis (C). (A) In vasculogenesis, circulating endothelial progenitor cells (EPC; purple) contribute to new blood vessel growth (capillaries). (B) During angiogenesis, endothelial cells are activated by ischemia and develop a lumen, thereby forming a new, small capillary vessel[3]. (C) In arteriogenesis, circulating leukocytes (green) are attracted to the activated endothelium. They assist in enlarging collateral anastomoses. Activated endothelial cells (blue), activated vascular smooth muscle cells (yellow)[3].

Normally, there is only a minimal net flow in these pre-existing connections. However, a sudden arterial occlusion or a slow progressing stenosis in the main artery can cause an increased pressure gradient in these small vessels to respond by actively proliferating and remodeling, which results in an increased lumen size and enhanced [perfusion to the ischemic tissue[20]. Hence, it seems that arteriogenesis is initiated differently and progresses differently from angiogenesis.]


3. Carmeliet, P., Mechanisms of angiogenesis and arteriogenesis. Nat Med, 2000. 6(4): p. 389-95.

6. van Oostrom, M.C., et al., Insights into mechanisms behind arteriogenesis: what does the future hold? J Leukoc Biol, 2008. 84(6): p. 1379-91.

20. Schaper, W. and D. Scholz, Factors regulating arteriogenesis. Arterioscler Thromb Vasc Biol, 2003. 23(7): p. 1143-51.

Haw 02a source.png

Fig. 1. Neovascularization can occur via vasculogenesis (A), angiogenesis (B), or arteriogenesis (C). (A) In vasculogenesis, circulating endothelial progenitor cells (EPC; purple) contribute to new blood vessel growth (capillaries) by secreting the necessary growth factors and chemokines for endothelial cells to migrate (upper) or by incorporating into the newly formed vessels (lower). (B) During angiogenesis, endothelial cells are activated by ischemia and grow in the direction of angiogenic signals. The endothelial cells fuse and develop a lumen, thereby forming a new, small capillary vessel. (C) In arteriogenesis, circulating leukocytes (green) are attracted to the activated endothelium. They assist in enlarging collateral anastomoses. Activated endothelial cells (blue), activated vascular smooth muscle cells (yellow), quiescent endothelial cells (gray), quiescent smooth muscle cells (brown).

[...]

Normally, as a result of the high resistance of arteriolar anastomoses and the lack of a pressure gradient, there is only a minimal net flow in these pre-existing connections. However, a sudden arterial occlusion or a slow progressing stenosis in the main artery can cause an increased pressure gradient in the anastomoses, leading to increased blood flow inside. These small vessels respond by actively proliferating and remodeling, which results in an increased lumen size and enhanced perfusion to the ischemic tissue [11]. Hence, it seems that arteriogenesis is initiated differently and progresses differently to angiogenesis.


11. Schaper, W., Scholz, D. (2003) Factors regulating arteriogenesis. Arterioscler. Thromb. Vasc. Biol. 23, 1143–1151.

Anmerkungen

Die Quelle ist für die Abbildung angegeben, nicht jedoch für die Bildunterschrift und den darauffolgenden Text. Auf die Bildunterschrift könnte man die Quellenangabe bei großzügiger Handhabung erstrecken, auf den Text schwerlich.

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[57.] Haw/Fragment 001 25 - Diskussion
Bearbeitet: 12. October 2014, 16:27 Schumann
Erstellt: 4. October 2014, 17:36 (Hindemith)
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The term “arteriogenesis”—the development of large collateral arteries from pre-existing arteriolar anastomoses—was proposed in 1997 by W. Schaper, R. Chapuli-Munoz, and W. Risau[7] to discriminate between arteriogenesis and true angiogenesis.

7. Ito, W.D., et al., Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am J Physiol, 1997. 273(3 Pt 2): p. H1255-65.

The term “arteriogenesis”—the development of large collateral arteries from pre-existing arteriolar anastomoses—was proposed in 1997 by W. Schaper, R. Chapuli-Munoz, and W. Risau [10] to discriminate between arteriogenesis and true angiogenesis.

10. Ito, W. D., Arras, M., Scholz, D., Winkler, B., Htun, P., Schaper, W. (1997) Angiogenesis but not collateral growth is associated with ischemia after femoral artery occlusion. Am. J. Physiol. 273, H1255–H1265.

Anmerkungen

Kein Verweis auf die Quelle

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[58.] Haw/Fragment 001 04 - Diskussion
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Cardiovascular disorders are currently the leading cause of death globally. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients who do not benefit from these treatment options. For a long time, it has been known that patients suffering from coronary heart disease can recruit collateral vessels and thereby improve symptoms of myocardial ischemia[1]. Also, it is well established that an increased demand for oxygen, as occurs during exercise and placental development, can induce formation of new capillaries[2]. Thus, it seems that the body already possesses an “in-house” rescue system to increase blood flow in ischemic circumstances. Stimulation of this system, termed neovascularization, could be a promising new direction in treating cardiovascular diseases[3]. Neovascularization in humans can be brought about by three distinct mechanisms: vasculogenesis, angiogenesis, or arteriogenesis (depicted in Fig. 1.1.)[3].

1. Helfant, R.H., P.S. Vokonas, and R. Gorlin, Functional importance of the human coronary collateral circulation. N Engl J Med, 1971. 284(23): p. 1277-81.

2. Prior, B.M., H.T. Yang, and R.L. Terjung, What makes vessels grow with exercise training? J Appl Physiol, 2004. 97(3): p. 1119-28.

3. Carmeliet, P., Mechanisms of angiogenesis and arteriogenesis. Nat Med, 2000. 6(4): p. 389-95.

In fact, cardiovascular disorders are currently the leading cause of death globally [1]. Although successful therapies exist to reduce plaque formation and restore blood flow in patients suffering from ischemic vascular diseases, there is still a significant portion of patients who do not benefit from these treatment options.

For a long time, it has been known that patients suffering from coronary heart disease can recruit collateral vessels and thereby improve symptoms of myocardial ischemia [2]. Also, it is well established that an increased demand in oxygen, as occurs during exercise and placental development, can induce formation of new capillaries [3]. Thus, it seems that the body already possesses an “in-house” rescue system to increase blood flow in ischemic circumstances. Stimulation of this system, termed neovascularization, could be a promising new direction in treating cardiovascular diseases. Neovascularization in humans can be fulfilled by three distinct mechanisms: vasculogenesis, angiogenesis, or arteriogenesis (depicted in Fig. 1) [4].


1. World Health Organization (February 2007) Factsheet 317.

2. Helfant, R. H., Vokonas, P. S., Gorlin, R. (1971) Functional importance of the human coronary collateral circulation. N. Engl. J. Med. 284, 1277–1281.

3. Prior, B. M., Yang, H. T., Terjung, R. L. (2004) What makes vessels grow with exercise training? J. Appl. Physiol. 97, 1119–1128.

4. Carmeliet, P. (2000) Mechanisms of angiogenesis and arteriogenesis. Nat. Med. 6, 389–395.

Anmerkungen

Ein Verweis auf die Quelle fehlt.

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