scholarly journals Upregulation of soluble vascular endothelial growth factor receptor type 1 by endogenous prostacyclin inhibitor coupling factor 6 in vascular endothelial cells: a role of acidosis-induced c-Src activation

2009 ◽  
Vol 32 (3) ◽  
pp. 182-187 ◽  
Author(s):  
Takashi Echizen ◽  
Tomohiro Osanai ◽  
Toshihiro Ashitate ◽  
Hiroaki Yokoyama ◽  
Shuji Shibutani ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Growth Factor Receptor ◽  
Coupling Factor ◽  
Vascular Endothelial ◽  
Endothelial Growth Factor ◽  
Coupling Factor 6

scholarly journals Lowering Caveolin-1 Expression in Human Vascular Endothelial Cells Inhibits Signal Transduction in Response to Shear Stress

2009 ◽  
Vol 2009 ◽  
pp. 1-9 ◽  
Author(s):  
A. D. van der Meer ◽  
M. M. J. Kamphuis ◽  
A. A. Poot ◽  
J. Feijen ◽  
I. Vermes
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Human Endothelial Cells ◽  
Caveolin 1 ◽  
Low Levels ◽  
Endothelial Growth Factor

Vascular endothelial cells have an extensive response to physiological levels of shear stress. There is evidence that the protein caveolin-1 is involved in the early phase of this response. In this study, caveolin-1 was downregulated in human endothelial cells by RNAi. When these cells were subjected to a shear stress of 15 dyn/cm2for 10 minutes, activation of Akt and ERK1/2 was significantly lower than in control cells. Moreover, activation of Akt and ERK1/2 in response to vascular endothelial growth factor was significantly lower in cells with low levels of caveolin-1. However, activation of integrin-mediated signaling during cell adhesion onto fibronectin was not hampered by lowered caveolin-1 levels. In conclusion, caveolin-1 is an essential component in the response of endothelial cells to shear stress. Furthermore, the results suggest that the role of caveolin-1 in this process lies in facilitating efficient VEGFR2-mediated signaling.

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