Fandom

VroniPlag Wiki

Haw/Fragment 008 01

< Haw

31.268Seiten in
diesem Wiki
Seite hinzufügen
Diskussion0 Share

Störung durch Adblocker erkannt!


Wikia ist eine gebührenfreie Seite, die sich durch Werbung finanziert. Benutzer, die Adblocker einsetzen, haben eine modifizierte Ansicht der Seite.

Wikia ist nicht verfügbar, wenn du weitere Modifikationen in dem Adblocker-Programm gemacht hast. Wenn du sie entfernst, dann wird die Seite ohne Probleme geladen.


Typus
BauernOpfer
Bearbeiter
Hindemith
Gesichtet
Yes.png
Untersuchte Arbeit:
Seite: 8, Zeilen: 1-19
Quelle: Schaper and Scholz 2003
Seite(n): 1146, Zeilen: l. Spalte: 2 ff.
[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.

Anmerkungen

Die Quelle wird in der Mitte der Übernahme erwähnt, ohne irgendeinen Hinweis, dass der gesamte Abschnitt aus ihr stammt.

Sichter
(Hindemith), SleepyHollow02

Auch bei Fandom

Zufälliges Wiki