Authors:
Li, X.;
Tjwa, M.;
Van Hove, I.;
Enholm, B.;
Neven, E.;
Paavonen, K.;
Jeltsch, M.;
Juan, T.D.;
Sievers, R.E.;
Chorianopoulos, E.;
Wada, H.;
Vanwildemeersch, M.;
Noel, A.;
Foidart, J.;
Springer, M.L.;
von De,Source:
Arteriosclerosis, Thrombosis, and Vascular Biology, Volume 28, p.1614-20 (2008)
URL:
http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed&Cmd=ShowDetailView&TermToSearch=18511699
Abstract:
OBJECTIVE: The endogenous role of the VEGF family member vascular endothelial growth factor-B (VEGF-B) in pathological angiogenesis remains unclear. METHODS AND RESULTS: We studied the role of VEGF-B in various models of pathological angiogenesis using mice lacking VEGF-B (VEGF-B(-/-)) or overexpressing VEGF-B(167). After occlusion of the left coronary artery, VEGF-B deficiency impaired vessel growth in the ischemic myocardium whereas, in wild-type mice, VEGF-B(167) overexpression enhanced revascularization of the infarct and ischemic border zone. By contrast, VEGF-B deficiency did not affect vessel growth in the wounded skin, hypoxic lung, ischemic retina, or ischemic limb. Moreover, VEGF-B(167) overexpression failed to enhance vascular growth in the skin or ischemic limb. CONCLUSIONS: VEGF-B appears to have a relatively restricted angiogenic activity in the ischemic heart. These insights might offer novel therapeutic opportunities.