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From the QCF Transgenic Laboratory and Human Genetics Laboratory, Joint Experimental Oncology Program, the Queensland Institute of Medical Research (D.B., G.U.S., C.A.P., M.G., A.M., M.M.C., I.D.T., S.M.G., S.T., N.K.H., G.F.K.), and the Department of Pathology, University of Queensland (M.C.C.), Brisbane, Australia; Griffith University (J.P.H.), Gold Coast Campus, Southport, Australia; Department of Cardiothoracic Surgery (P.S.T.), Imperial College School of Medicine, National Heart and Lung Institute, London, UK; and Centre for Molecular and Cellular Biology (C.W., M.L.), University of Queensland, Brisbane, Australia.
Correspondence to Graham Kay, Queensland Institute of Medical Research, Post Office Royal Brisbane Hospital, Queensland 4029, Australia. E-mail grahamK{at}qimr.edu.au
AbstractVascular endothelial growth factor-B (VEGF-B) is closely related to VEGF-A, an effector of blood vessel growth during development and disease and a strong candidate for angiogenic therapies. To further study the in vivo function of VEGF-B, we have generated Vegfb knockout mice (Vegfb-/-). Unlike Vegfa knockout mice, which die during embryogenesis, Vegfb-/- mice are healthy and fertile. Despite appearing overtly normal, Vegfb-/- hearts are reduced in size and display vascular dysfunction after coronary occlusion and impaired recovery from experimentally induced myocardial ischemia. These findings reveal a role for VEGF-B in the development or function of coronary vasculature and suggest potential clinical use in therapeutic angiogenesis. The full text of this article is available at http://www.circresaha.org.
Key Words: angiogenesis cardiac ischemia coronary vasculature
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