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Published March 2002 | Published
Journal Article Open

Cardiovascular ephrinB2 function is essential for embryonic angiogenesis


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.

Additional Information

© 2002 The Company of Biologists Limited. Accepted December 19, 2001. We thank T. Sato for the generous gift of Tie2-Cre transgenic mice, Emma Dormand for assistance with in situ hybridization techniques, Shirley Pease and the staff of the Transgenic Animal Facility at Caltech for assistance with animal husbandry, Gabriele Mosconi for laboratory management, Joanna Yamada for technical support, and Gina Mancuso for administrative assistance. D. J. A. is an Investigator of the Howard Hughes Medical Institute. This work was supported by NIH grant #HL-66221-02 and American Heart Association grant #9950157N.

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