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Angiogenesis is a complex process orchestrated by both growth factors and cell adhesion and is initiated by focal degradation of the vascular basement membrane with subsequent migration and proliferation of endothelial cells. The Ras/Raf/MEK/ERK pathway is required for EC function during angiogenesis. Although  in vitro  studies implicate ERK1 and ERK2 in endothelial cell survival, their precise role in angiogenesis  in vivo  remains poorly defined.  Cre/loxP  technology was used to inactivate  Erk1  and  Erk2  in endothelial cells during murine development, resulting in embryonic lethality due to severely reduced angiogenesis. Deletion of  Erk1  and  Erk2  in primary endothelial cells resulted in decreased cell proliferation and migration, but not in increased apoptosis. Expression of key cell cycle regulators was diminished in the double knockout cells, and decreased DNA synthesis could be observed in endothelial cells during embryogenesis. Interestingly, both Paxillin and Focal Adhesion Kinase were expressed at lower levels in endothelial cells lacking  Erk1  and  Erk2  both  in vivo  and  in vitro , leading to defects in the organization of the cytoskeleton and in cell motility. The regulation of Paxillin and Focal Adhesion Kinase expression occurred post-transcriptionally. These results demonstrate that ERK1 and ERK2 coordinate endothelial cell proliferation and migration during angiogenesis.

Erk1 and Erk2 Regulate Endothelial Cell Proliferation and Migration during Mouse Embryonic Angiogenesis