Activation of mitogen-activated protein kinases by vascular endothelial growth factor and basic fibroblast growth factor in capillary endothelial cells is inhibited by the antiangiogenic factor 16-kDa N-terminal fragment of prolactin

摘要: A number of factors both stimulating and inhibiting angiogenesis have been described. In the current work, we demonstrate that angiogenic factor vascular endothelial growth (VEGF) activates mitogen-activated protein kinase (MAPK) as has previously shown for basic fibroblast factor. The antiagiogenic 16-kDa N-terminal fragment human prolactin inhibits activation MAPK distal to autophosphorylation putative VEGF receptor, Flk-1, phospholipase C-gamma. These data show inhibition may play a central role in control angiogenesis.