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      Vascular endothelial growth factor induces expression of the antiapoptotic proteins Bcl-2 and A1 in vascular endothelial cells.

      The Journal of Biological Chemistry
      Apoptosis, genetics, Base Sequence, Cell Survival, Cells, Cultured, Culture Media, Serum-Free, DNA Primers, Endothelial Growth Factors, metabolism, Endothelium, Vascular, cytology, Genes, bcl-2, Humans, Lymphokines, Vascular Endothelial Growth Factor A, Vascular Endothelial Growth Factors

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          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.

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