SEARCH:   Advanced

Blood, 1 March 2007, Vol. 109, No. 5, pp. 1962-1970. Prepublished online as a Blood First Edition Paper on October 24, 2006; DOI 10.1182/blood-2005-10-038893. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2005-10-038893v1 109/5/1962    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 HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Weis, S. M. Articles by Cheresh, D. A. Search for Related Content PubMed PubMed Citation Articles by Weis, S. M. Articles by Cheresh, D. A. Related Collections Cell Adhesion and Motility Signal Transduction Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Cooperation between VEGF and ß3 integrin during cardiac vascular development Sara M. Weis1, Jeffrey N. Lindquist1, Leo A. Barnes1, Kimberly M. Lutu-Fuga1, Jianhua Cui1, Malcolm R. Wood2, and David A. Cheresh1 1 Moores UCSD Cancer Center, University of California, San Diego; 2 Core Microscopy Facility, The Scripps Research Institute, La Jolla, CA In the developing myocardium, vascular endothelial growth factor (VEGF)–dependent neovascularization occurs by division of existing vessels, a process that persists for several weeks following birth. During this remodeling phase, mRNA expression of ß3 integrin in the heart decreases significantly as vessel maturation progresses. However, in male mice lacking ß3, coronary capillaries fail to mature and continue to exhibit irregular endothelial thickness, endothelial protrusions into the lumen, and expanded cytoplasmic vacuoles. Surprisingly, this phenotype was not seen in female ß3-null mice. Enhanced VEGF signaling contributes to the ß3-null phenotype, because these vessels can be normalized by inhibitors of VEGF or Flk-1. Moreover, intravenous injection of VEGF induces a similar angiogenic phenotype in hearts of adult wild-type mice. These findings show a clear vascular phenotype in the hearts of mice lacking ß3 and suggest this integrin plays a critical role in coronary vascular development and the vascular response to VEGF. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: W. Yan, B. Bentley, and R. Shao Distinct Angiogenic Mediators Are Required for Basic Fibroblast Growth Factor- and Vascular Endothelial Growth Factor-induced Angiogenesis: The Role of Cytoplasmic Tyrosine Kinase c-Abl in Tumor Angiogenesis Mol. Biol. Cell, May 1, 2008; 19(5): 2278 - 2288. [Abstract] [Full Text] [PDF] G. Serini, L. Napione, M. Arese, and F. Bussolino Besides adhesion: new perspectives of integrin functions in angiogenesis Cardiovasc Res, May 1, 2008; 78(2): 213 - 222. [Abstract] [Full Text] [PDF] E. Brakenhielm Substrate Matters: Reciprocally Stimulatory Integrin and VEGF Signaling in Endothelial Cells Circ. Res., September 14, 2007; 101(6): 536 - 538. [Full Text] [PDF] G. H. Mahabeleshwar, W. Feng, K. Reddy, E. F. Plow, and T. V. Byzova Mechanisms of Integrin Vascular Endothelial Growth Factor Receptor Cross-Activation in Angiogenesis Circ. Res., September 14, 2007; 101(6): 570 - 580. [Abstract] [Full Text] [PDF] E. C. Miller, B. E. Capps, R. R. Sanghani, D. R. Clemmons, and L. A. Maile Regulation of IGF-I Signaling in Retinal Endothelial Cells by Hyperglycemia Invest. Ophthalmol. Vis. Sci., August 1, 2007; 48(8): 3878 - 3887. [Abstract] [Full Text] [PDF]

	Blood Online is supported in part by Genentech BioOncology and Biogen Idec
	Copyright © 2007 by American Society of Hematology         Online ISSN: 1528-0020