Defective angiogenesis, endothelial migration, proliferation, and MAPK signaling in Rap1b-deficient mice.

ABSTRACT: Angiogenesis is the main mechanism of vascular remodeling during late development and, after birth, in wound healing. Perturbations of angiogenesis occur in cancer, diabetes, ischemia, and inflammation. While much progress has been made in identifying factors that control angiogenesis, the understanding of the precise molecular mechanisms involved is incomplete. Here we identify a small GTPase, Rap1b, as a positive regulator of angiogenesis. Rap1b-deficient mice had a decreased level of Matrigel plug and neonatal retinal neovascularization, and aortas isolated from Rap1b-deficient animals had a reduced microvessel sprouting response to 2 major physiological regulators of angiogenesis: vascular endothelial growth factor (VEGF) and basic fibroblasts growth factor (bFGF), indicating an intrin

SUBMITTER: Chrzanowska-Wodnicka M 

PROVIDER: S-EPMC2254536 | biostudies-literature | 2008 Mar

REPOSITORIES: biostudies-literature