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Blood, 1 April 2005, Vol. 105, No. 7, pp. 2771-2776. Prepublished online as a Blood First Edition Paper on December 16, 2004; DOI 10.1182/blood-2004-06-2244. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-06-2244v1 105/7/2771    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Crosby, C. V. Articles by Drake, C. J. Search for Related Content PubMed PubMed Citation Articles by Crosby, C. V. Articles by Drake, C. J. Related Collections Hemostasis, Thrombosis, and Vascular Biology Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY VE-cadherin is not required for the formation of nascent blood vessels but acts to prevent their disassembly Christopher V. Crosby, Paul A. Fleming, W. Scott Argraves, Monica Corada, Lucia Zanetta, Elisabetta Dejana, and Christopher J. Drake From the Cardiovascular Developmental Biology Center, Department of Cell Biology, Medical University of South Carolina, Charleston, SC; and Department of Vascular Biology, Italian Foundation for Cancer Research (FIRC), Institute of Molecular Oncology, Milan, Italy. We investigated the role of vascular endothelial (VE)–cadherin in blood vessel morphogenesis and established a temporal correlation linking the failure in vessel morphogenesis in VE-cadherin null embryos to a specific step in vasculogenesis. We showed that the sequence in which blood vessels failed followed the order in which they had formed (ie, those forming first—yolk sac, allantoic and endocardial vessels—were the first to display morphologic abnormalities). We next showed that in place of normal reticulated networks of blood vessels, clusters of platelet endothelial cell adhesion molecule–positive (PECAM+) cells formed within cultured allantois explants from VE-cadherin null embryos. Similarly, a function-blocking VE-cadherin antibody, BV13, caused PECAM+ cell clusters to form in cultured allantois explants from normal mice. Finally, we demonstrated that formation of PECAM+ cell clusters in response to BV13 was not due to a disruption in the formation of nascent vessels but was due to the actual disassembly of nascent vessels. Based on these findings, we conclude that the events of de novo blood vessel formation up to the point at which a vascular epithelium forms (ie, nascent vessels with lumens) are not dependent on VE-cadherin and that VE-cadherin, whose expression is up-regulated following vascular epithelialization, is required to prevent the disassembly of nascent blood vessels. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

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