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Originally published In Press as doi:10.1074/jbc.M004994200 on August 4, 2000

J. Biol. Chem., Vol. 275, Issue 43, 33679-33687, October 27, 2000
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Maintenance of Vascular Integrity in the Embryo Requires Signaling through the Fibroblast Growth Factor Receptor*

Sang Hoon Lee, Derrick J. Schloss, and Judith L. SwainDagger

From the Department of Medicine, Stanford University School of Medicine, Stanford, California 94305-5109

Basic fibroblast growth factor (FGF)-2 is important for vessel formation and/or maintenance of vascular integrity in the embryo. FGF signaling may be mediated through transmembrane tyrosine kinase receptors or directly through intracellular pathways that do not involve receptor activation. To determine the role of receptor-mediated signaling in endothelial cells, an adenovirus encoding truncated FGF receptor (FGFR)-1, under the control of the cytomegalovirus promoter, was expressed in endothelial cells. FGF signaling was impaired, as indicated by inhibition of MAPK phosphorylation. Functional consequences included inhibition of endothelial cell migration and induction of apoptosis. To address the role of endothelial FGFR signaling in vascular development, recombinant adenovirus encoding a dominant-negative FGFR was injected into the sinus venosus of embryonic day 9.0 cultured mouse embryos. Previous studies demonstrated that transgenes delivered via adenovirus, under the control of the cytomegalovirus promoter, are expressed selectively in the developing vasculature. Embryos expressing a control adenovirus developed normally, whereas those expressing the FGFR-1 mutant exhibited abnormal embryonic and extra-embryonic vascular development. These data demonstrate that FGF, by signaling through the FGFR, plays a pivotal role in the development and maintenance of a mature vascular network in the embryo.

* This work was supported by National Institutes of Health Grants HL26831 (to J. L. S.) and T32 HL07708 (to S. H. L.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger To whom correspondence should be addressed: Dept. of Medicine, S-102, Stanford University, 300 Pasteur Dr., Stanford, CA 94305-5109. Tel.: 650-489-7778; Fax: 650-725-8381; E-mail: jlswain@stanford.edu.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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