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Autor     Wolfgang Schaper, Dimitri Scholz
Titel    Factors Regulating Arteriogenesis
Zeitschrift    Arteriosclerosis, Thrombosis, and Vascular Biology
Herausgeber    American Heart Association
Ausgabe    23
Jahr    2003
Seiten    1143-1151
ISSN    1524-4636
DOI    10.1161/01.ATV.0000069625.11230.96
URL    http://atvb.ahajournals.org/content/23/7/1143.full.pdf

Literaturverz.   

ja
Fußnoten    ja
Fragmente    9


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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.

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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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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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[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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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 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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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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[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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[9.] Haw/Fragment 015 02 - Diskussion
Zuletzt bearbeitet: 2014-10-17 17:14:55 Singulus
BauernOpfer, Fragment, Gesichtet, Haw, SMWFragment, Schaper and Scholz 2003, Schutzlevel sysop

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Quelle: Schaper and Scholz 2003
Seite(n): 1150, Zeilen: 6ff
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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