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Present address: Department of Developmental Neurobiology, NIMR, The RIdgeway, Mill Hill, London NW7 1AA, UK
1 Division of Biology 216-76, California Institute of Technology, Pasadena, CA 91125, USA
2 Howard Hughes Medical Institute, California Institute of Technology, Pasadena, CA 91125, USA
*Author for correspondence (e-mail: c/o mancusog{at}cco.caltech.edu)
Accepted 19 December 2001
EphrinB2, a transmembrane ligand of EphB receptor tyrosine kinases, is specifically expressed in arteries. In ephrinB2 mutant embryos, there is a complete arrest of angiogenesis. However, ephrinB2 expression is not restricted to vascular endothelial cells, and it has been proposed that its essential function may be exerted in adjacent mesenchymal cells. We have generated mice in which ephrinB2 is specifically deleted in the endothelium and endocardium of the developing vasculature and heart. We find that such a vascular-specific deletion of ephrinB2 results in angiogenic remodeling defects identical to those seen in the conventional ephrinB2 mutants. These data indicate that ephrinB2 is required specifically in endothelial and endocardial cells for angiogenesis, and that ephrinB2 expression in perivascular mesenchyme is not sufficient to compensate for the loss of ephrinB2 in these vascular cells.
Key words: EphB4, EphrinB2, Angiogenesis, Vasculature, Mouse
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