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Arteriogenesis in Gja5 (Connexin-40) deficient mice

von Dr. Haitao Wang

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[1.] Haw/Fragment 002 01 - Diskussion
Zuletzt bearbeitet: 2014-10-15 19:02:19 Singulus
Fragment, Gesichtet, Haw, KomplettPlagiat, Limbourg et al 2009, SMWFragment, Schutzlevel sysop

Typus
KomplettPlagiat
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 2, Zeilen: 1-6
Quelle: Limbourg et al 2009
Seite(n): 1737, Zeilen: l. Spalte: 19ff
[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).

Anmerkungen

Ein Verweis auf die Quelle fehlt.

Sichter
(Hindemith) Klgn

[2.] Haw/Fragment 002 07 - Diskussion
Zuletzt bearbeitet: 2014-10-12 16:29:43 Schumann
BauernOpfer, Fragment, Gesichtet, Haw, SMWFragment, Schutzlevel sysop, Van Oostrom et al 2008

Typus
BauernOpfer
Bearbeiter
Hindemith
Gesichtet
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Untersuchte Arbeit:
Seite: 2, Zeilen: 7-16
Quelle: Van Oostrom et al 2008
Seite(n): 1380, Zeilen: Figure 1, l.Sp. 13 ff.
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.

Sichter
(Hindemith), SleepyHollow02


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