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

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