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Arteriogenesis in Gja5 (Connexin-40) deficient mice

von Dr. Haitao Wang

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[1.] Haw/Fragment 011 01 - Diskussion
Zuletzt bearbeitet: 2014-10-17 09:31:50 Singulus
BauernOpfer, Fragment, Gesichtet, Haw, SMWFragment, Schaper and Scholz 2003, Schutzlevel sysop

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Untersuchte Arbeit:
Seite: 11, Zeilen: 1-24
Quelle: Schaper and Scholz 2003
Seite(n): 1148, 1149, Zeilen: 1148: r. Spalte: 44ff; 1149: l. Spalte: 1ff
[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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Auf die Quelle wird zweimal verwiesen, es wird aber nicht klar, dass die gesamte Passage inkl. einiger Literaturverweise aus der Quelle stammt.

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