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Papers In Press, published online ahead of print December 20, 2001
Molecular Oncology, Genentech Inc., South San Francisco, CA 94080
Corresponding Author: nf{at}gene.com
EG-VEGF has been recently identified as a mitogen specific for the endothelium of steroidogenic glands. Here we report a characterization of the signal transduction of EG-VEGF in a responsive cell type, bovine adrenal cortex endothelial (ACE) cells. EG-VEGF led to a time- and dose-dependent phosphorylation of p44/42 MAPK. This effect was blocked by pre-treatment with pertussis toxin, suggesting that Gai plays an important role in mediating EG-VEGF induced activation of MAPK signaling. The inhibitor of p44/42 MAPK phosphorylation PD 98059 resulted in suppression of both proliferation and migration in response to EG-VEGF. EG-VEGF also increased the phosphorylation of Akt in a PI-3 kinase-dependent manner. Consistent with such effect, EG-VEGF was a potent survival factor for ACE cells. We also identified endothelial nitric oxidase (eNOS) as one of the downstream targets of Akt activation. Phosphorylation of eNOS in ACE cells was stimulated by EG-VEGF with a time course correlated to the Akt phosphorylation . Our data demonstrate that EG-VEGF, possibly through binding to a GPCR, results in the activation of MAPK p44/42 and PI 3-kinase signaling pathways, leading to proliferation, migration and survival of responsive endothelial cells.
J. Biol. Chem, 10.1074/jbc.M110594200
Submitted on November 4, 2001
Revised on December 12, 2001
Accepted on December 19, 2001
Characterization of EG-VEGF signaling in adrenal cortex-derived capillary endothelial cells
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