J. Cell Biol., Volume 140, Number 5, March 9, 1998 1255-1263

Integrin v3 Requirement for Sustained Mitogen-activated Protein Kinase Activity during Angiogenesis

Brian P. Eliceiri, Richard Klemke, Staffan Strömblad, and David A. Cheresh

Departments of Immunology and Vascular Biology, The Scripps Research Institute, La Jolla, California 92037

Angiogenesis depends on growth factors and vascular cell adhesion events. Integrins and growth factors are capable of activating the ras/MAP kinase pathway in vitro, yet how these signals influence endothelial cells during angiogenesis is unknown. Upon initiation of angiogenesis with basic fibroblast growth factor (bFGF) on the chick chorioallantoic membrane (CAM), endothelial cell mitogen-activated protein (MAP) kinase (ERK) activity was detected as early as 5 min yet was sustained for at least 20 h. The initial wave of ERK activity (5-120 min) was refractory to integrin antagonists, whereas the sustained activity (4-20 h) depended on integrin v3, but not 1 integrins. Inhibition of MAP kinase kinase (MEK) during this sustained v3-dependent ERK signal blocked the formation of new blood vessels while not influencing preexisting blood vessels on the CAM. Inhibition of MEK also blocked growth factor induced migration but not adhesion of endothelial cells in vitro. Therefore, angiogenesis depends on sustained ERK activity regulated by the ligation state of both a growth factor receptor and integrin v3.

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