Abstract

We examined the role of vascular endothelial growth factor (VEGF) in preventing apoptosis in primary human umbilical vein endothelial (HUVE) cells. VEGF was capable of preventing serum starvation-induced apoptosis at concentrations between 10 and 100 ng/ml. The addition of VEGF to serum-starved HUVE cells led to a 5. 2-fold induction of Bcl-2 after 36 h and to a transient, 2.4-fold induction of A1 after a 7-h incubation, as quantitated by real time reverse transcriptase-polymerase chain reaction analysis. Western blot analysis demonstrated a 2-3-fold induction of Bcl-2 protein after 18-36 h of exposure to VEGF and a transient induction of A1 after 7 h of VEGF stimulation. Moreover, overexpression of Bcl-2 by means of transient biolistic transfection experiments of HUVE cells was sufficient to prevent endothelial cells from apoptotic cell death in the absence of VEGF. These findings indicate that Bcl-2 plays an important role in mediating the survival activity of VEGF on endothelial cells.

Keywords

Vascular endothelial growth factor BVascular endothelial growth factor CCell biologyVascular endothelial growth factor AVascular endothelial growth factorChemistryBiologyCancer researchVEGF receptors

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Year
1998
Type
article
Volume
273
Issue
21
Pages
13313-13316
Citations
988
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Hans‐Peter Gerber, Vishva M. Dixit, Napoleone Ferrara (1998). Vascular Endothelial Growth Factor Induces Expression of the Antiapoptotic Proteins Bcl-2 and A1 in Vascular Endothelial Cells. Journal of Biological Chemistry , 273 (21) , 13313-13316. https://doi.org/10.1074/jbc.273.21.13313

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DOI
10.1074/jbc.273.21.13313