Article

Selective requirement for Src kinases during VEGF-induced angiogenesis and vascular permeability.

Department of Immunology, Scripps Research Institute, La Jolla, California 92037, USA.
Molecular Cell (Impact Factor: 14.46). 01/2000; 4(6):915-24. DOI: 10.1016/S1097-2765(00)80221-X
Source: PubMed

ABSTRACT Src kinase activity was found to protect endothelial cells from apoptosis during vascular endothelial growth factor (VEGF)-, but not basic fibroblast growth factor (bFGF)-, mediated angiogenesis in chick embryos and mice. In fact, retroviral targeting of kinase-deleted Src to tumor-associated blood vessels suppressed angiogenesis and the growth of a VEGF-producing tumor. Although mice lacking individual Src family kinases (SFKs) showed normal angiogenesis, mice deficient in pp60c-src or pp62c-yes showed no VEGF-induced vascular permeability (VP), yet fyn-/- mice displayed normal VP. In contrast, inflammation-mediated VP appeared normal in Src-deficient mice. Therefore, VEGF-, but not bFGF-, mediated angiogenesis requires SFK activity in general, whereas the VP activity of VEGF specifically depends on the SFKs, Src, or Yes.

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