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Blood, 1 February 2005, Vol. 105, No. 3, pp. 1094-1101. Prepublished online as a Blood First Edition Paper on September 30, 2004; DOI 10.1182/blood-2004-06-2315. This Article Full Text Full Text (PDF) All Versions of this Article: 2004-06-2315v1 105/3/1094    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 Berger, M. Articles by Ganss, R. Search for Related Content PubMed PubMed Citation Articles by Berger, M. Articles by Ganss, R. Related Collections Hemostasis, Thrombosis, and Vascular Biology Neoplasia Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Regulator of G-protein signaling-5 induction in pericytes coincides with active vessel remodeling during neovascularization Mario Berger, Gabriele Bergers, Bernd Arnold, Günter J. Hämmerling, and Ruth Ganss From the Department of Molecular Immunology, German Cancer Research Center, Heidelberg, Germany; and Department of Neurological Surgery, Brain Tumor Research Center (BTRC), University of California Comprehensive Cancer Center, San Francisco, CA. We identified regulator of G-protein signaling-5 (RGS-5) as an angiogenic pericyte marker at sites of physiologic and pathologic angiogenesis. In a mouse model of pancreatic islet cell carcinogenesis, RGS-5 is specifically induced in the vasculature of premalignant lesions during the "angiogenic switch" and further elevated in tumor vessels. Similarly, RGS-5 is overexpressed in highly angiogenic astrocytomas but not in hypoxia-inducible factor-1 (HIF-1)–deficient tumors, which grow along preexisting brain capillaries without inducing neovessels. Elevated levels of RGS-5 in pericytes are also observed during wound healing and ovulation indicating a strong correlation between RGS-5 expression and active vessel remodeling beyond tumor angiogenesis. Moreover, antitumor therapy, which reverses tumor vasculature to an almost normal morphology, results in down-regulation of RGS-5 transcription. Taken together, these data demonstrate for the first time a factor that is specific for "activated" pericytes. This further supports the notion that pericytes, like endothelial cells, undergo molecular changes during neovascularization that makes them a novel target for antiangiogenic therapy. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Jin, X. An, Z. Ye, B. Cully, J. Wu, and J. Li RGS5, a Hypoxia-inducible Apoptotic Stimulator in Endothelial Cells J. Biol. Chem., August 28, 2009; 284(35): 23436 - 23443. [Abstract] [Full Text] [PDF] K. Gaengel, G. Genove, A. Armulik, and C. Betsholtz Endothelial-Mural Cell Signaling in Vascular Development and Angiogenesis Arterioscler Thromb Vasc Biol, May 1, 2009; 29(5): 630 - 638. [Abstract] [Full Text] [PDF] M. Manzur, J. Hamzah, and R. Ganss Modulation of G Protein Signaling Normalizes Tumor Vessels Cancer Res., January 15, 2009; 69(2): 396 - 399. 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