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Mice Lacking the Vascular Endothelial Growth Factor-B Gene ( Vegfb ) Have Smaller Hearts, Dysfunctional Coronary Vasculature, and Impaired Recovery From Cardiac Ischemia
Author(s) -
Daniela Bellomo,
John P. Headrick,
Ginters Silins,
Carol Paterson,
Penny S. Thomas,
Michael G. Gartside,
Arne W. Mould,
Marian M. Cahill,
Ian D. Tonks,
Sean M. Grimmond,
Steve Townson,
Christine A. Wells,
Melissa H. Little,
Margaret C. Cummings,
Nicholas K. Hayward,
Graham F. Kay
Publication year - 2000
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/01.res.86.2.e29
Subject(s) - angiogenesis , vascular endothelial growth factor b , vascular endothelial growth factor , knockout mouse , vascular endothelial growth factor a , vascular endothelial growth factor c , ischemia , medicine , biology , receptor , vegf receptors
Vascular 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.

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