SEARCH:   Advanced

Blood, 1 February 2007, Vol. 109, No. 3, pp. 987-994. Prepublished online as a Blood First Edition Paper on October 10, 2006; DOI 10.1182/blood-2006-07-036400. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-07-036400v1 109/3/987    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 Ma, J. Articles by Chen, Y.-G. Search for Related Content PubMed PubMed Citation Articles by Ma, J. Articles by Chen, Y.-G. Related Collections Cell Adhesion and Motility Hemostasis, Thrombosis, and Vascular Biology Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY MCP-1 mediates TGF-ß–induced angiogenesis by stimulating vascular smooth muscle cell migration Jing Ma1, Qiang Wang1, Teng Fei1, Jing-Dong Jackie Han2, and Ye-Guang Chen1 From the1 State Key Laboratory of Biomembrane and Membrane Biotechnology, Department of Biological Sciences and Biotechnology, Tsinghua University, Beijing, China; and 2 Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China Transforming growth factor-ß (TGF-ß) and its signaling mediators play crucial roles in vascular formation. Our previous microarray analysis identified monocyte chemoattractant protein-1 (MCP-1) as a TGF-ß target gene in endothelial cells (ECs). Here, we report that MCP-1 mediates the angiogenic effect of TGF-ß by recruiting vascular smooth muscle cells (VSMCs) and mesenchymal cells toward ECs. By using a chick chorioallantoic membrane assay, we show that TGF-ß promotes the formation of new blood vessels and this promotion is attenuated when MCP-1 activity is blocked by its neutralizing antibody. Wound healing and transwell assays established that MCP-1 functions as a chemoattractant to stimulate migration of VSMCs and mesenchymal 10T1/2 cells toward ECs. Furthermore, the conditioned media from TGF-ß–treated ECs stimulate VSMC migration, and inhibition of MCP-1 activity attenuates TGF-ß–induced VSMC migration toward ECs. Finally, we found that MCP-1 is a direct gene target of TGF-ß via Smad3/4. Taken together, our findings suggest that MCP-1 mediates TGF-ß–stimulated angiogenesis by enhancing migration of mural cells toward ECs and thus promoting the maturation of new blood vessels. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: MCP-1 muscles in on pericytes Simon Karpatkin Blood 2007 109: 849-850. [Full Text] [PDF] This article has been cited by other articles: T. Kinnaird, E. Stabile, S. Zbinden, M.-S. Burnett, and S. E. Epstein Cardiovascular risk factors impair native collateral development and may impair efficacy of therapeutic interventions Cardiovasc Res, May 1, 2008; 78(2): 257 - 264. [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