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Research results from Blood Research Institute update understanding of angiogenesis
April 7th, 2008
2008 APR 7 -- A report, 'Defective angiogenesis, endothelial migration, proliferation, and MAPK signaling in Rap1b-deficient mice,' is newly published data in Blood. According to recent research published in the journal Blood, "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 intrinsic defect in endothelial cells. Proliferation of retinal endothelial cells in situ and in vitro migration of lung endothelial cells isolated from Rap1b-deficient mice were inhibited. At the molecular level, activation of 2 MAP kinases, p38 MAPK and p42/44 ERK, important regulators of endothelial migration and proliferation, was decreased in Rap1b-deficient endothelial cells in response to VEGF stimulation," wrote M. Chrzanowska-Wodnicka and colleagues, Blood Research Institute. The researchers concluded: "These studies provide evidence that Rap1b is required for normal angiogenesis and reveal a novel role of Rap1 in regulation of proangiogenic signaling in endothelial cells." Chrzanowska-Wodnicka and colleagues published their study in Blood (Defective angiogenesis, endothelial migration, proliferation, and MAPK signaling in Rap1b-deficient mice. Blood, 2008;111(5):2647-56). For additional information, contact M. Chrzanowska-Wodnicka, Blood Research Institute, BloodCenter of Wisconsin, Milwaukee, WI 53201 USA.. The publisher's contact information for the journal Blood is: American Society Hematology, 1900 M Street. NW Suite 200, Washington, DC 20036, USA. Keywords: United States, Milwaukee, Angiogenesis, Cancer, Diabetes, Inflammation, Ischemia, Oncology, Physiology, Retinal Neovascularization, Tumor Vascularization. This article was prepared by Clinical Oncology Week editors from staff and other reports. Copyright 2008, Clinical Oncology Week via NewsRx.com.
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