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Blood, 1 April 2007, Vol. 109, No. 7, pp. 2847-2853. Prepublished online as a Blood First Edition Paper on November 21, 2006; DOI 10.1182/blood-2006-08-039743. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-08-039743v1 109/7/2847    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 Ren, R. Articles by Patterson, C. Search for Related Content PubMed PubMed Citation Articles by Ren, R. Articles by Patterson, C. Related Collections Hemostasis, Thrombosis, and Vascular Biology Gene Expression Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Gene expression profiles identify a role for cyclooxygenase 2–dependent prostanoid generation in BMP6-induced angiogenic responses Rongqin Ren1, Peter C. Charles1,2, Chunlian Zhang1, Yaxu Wu1, Hong Wang1, and Cam Patterson1,2 1 Carolina Cardiovascular Biology Center and 2 Department of Medicine, University of North Carolina, Chapel Hill The bone morphogenetic protein (BMP) family of proteins participates in regulation of angiogenesis in physiologic and pathologic conditions. To investigate the molecular mechanisms that contribute to BMP-dependent angiogenic signaling, we performed gene expression profiling of BMP6-treated mouse endothelial cells. We detected 77 mRNAs that were differentially regulated after BMP6 stimulation. Of these, cyclooxygenase 2 (Cox2) was among the most highly up-regulated by BMP stimulation, suggesting a role for Cox2 as a downstream regulator of BMP-induced angiogenesis. Up-regulation of Cox2 by BMP6 was detected at both mRNA and protein levels in endothelial cells, and BMP6 increased production of prostaglandins in a Cox2-dependent fashion. BMP6 up-regulated Cox2 at the transcriptional level through upstream SMAD-binding sites in the Cox2 promoter. Pharmacologic inhibition of Cox2, but not Cox1, blocked BMP6-induced endothelial cell proliferation, migration, and network assembly. BMP6-dependent microvessel outgrowth was markedly attenuated in aortic rings from Cox2–/– mice or after pharmacologic inhibition of Cox2 in aortas from wild-type mice. These results support a necessary role for Cox2 in mediating proangiogenic activities of BMP6. These data indicate that Cox2 may serve as a unifying component downstream from disparate pathways to modulate angiogenic responses in diseases in which neovascularization plays an underlying pathophysiologic role. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: X. Pi, R. Ren, R. Kelley, C. Zhang, M. Moser, A. B. Bohil, M. DiVito, R. E. Cheney, and C. Patterson Sequential roles for myosin-X in BMP6-dependent filopodial extension, migration, and activation of BMP receptors J. Cell Biol., December 31, 2007; 179(7): 1569 - 1582. [Abstract] [Full Text] [PDF]

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