scholarly journals Protein kinase C   promotes angiogenic activity of human endothelial cells via induction of vascular endothelial growth factor

2008 ◽  
Vol 78 (2) ◽  
pp. 349-355 ◽  
Author(s):  
H. Xu ◽  
P. Czerwinski ◽  
M. Hortmann ◽  
H.-Y. Sohn ◽  
U. Forstermann ◽  
...  
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Vascular Endothelial ◽  
Human Endothelial Cells ◽  
Angiogenic Activity ◽  
Kinase C ◽  
Endothelial Growth Factor

Vascular Endothelial Growth Factor Enhances the Expression of Urokinase Receptor in Human Endothelial Cells via Protein Kinase C Activation

2001 ◽  
Vol 85 (02) ◽  
pp. 296-302 ◽  
Author(s):  
Marielle Kroon ◽  
Pieter Koolwijk ◽  
Mario Vermeer ◽  
Bea van der Vecht ◽  
Victor van Hinsbergh
Keyword(s):  
Vascular Endothelial Growth Factor ◽  
Endothelial Cells ◽  
Protein Kinase C ◽  
Growth Factor ◽  
Protein Kinase ◽  
Receptor Expression ◽  
Vascular Endothelial ◽  
Human Endothelial Cells ◽  
Kinase C ◽  
Endothelial Growth Factor

SummaryAmong other proteolytic enzymes, the urokinase-type plasminogen activator (u-PA)/plasmin cascade contributes to cell migration and the formation of capillary-like structures in a fibrinous exudate. The u-PA receptor (u-PAR) focuses proteolytical activity on the cell surface of the endothelial cell and hereby accelerates the pericellular matrix degradation. Vascular endothelial growth factor (VEGF) and fibroblast growth factor (FGF)-2 enhance u-PA receptor expression in human endothelial cells. In this paper we show that the protein kinase C (PKC) inhibitors Ro31-8220 and GF109203X inhibit VEGF165-induced u-PAR antigen expression in human endothelial cells, whereas PKC inhibition had no effect on FGF-2-induced u-PAR antigen enhancement. In addition, inhibition of PKC activity had no effect on VEGF165-or FGF-2-induced proliferation in human endothelial cells. We conclude that VEGF165 induces u-PAR via a PKC-dependent pathway, whereas proliferation is induced via a different pathway probably involving tyrosine phosphorylation of proteins downstream of the VEGF receptors.

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