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| Untersuchte Arbeit: Seite: 6, Zeilen: 1-9 |
Quelle: Schaper 2009 Seite(n): 7, Zeilen: r. Spalte: 33ff |
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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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