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Blood, 7 May 2009, Vol. 113, No. 19, pp. 4810-4818. Prepublished online as a Blood First Edition Paper on February 9, 2009; DOI 10.1182/blood-2008-07-170316. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: blood-2008-07-170316v1 113/19/4810    most recent Alert me when this article is cited Alert me if a correction is posted 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 Kimura, H. Articles by Sato, Y. Search for Related Content PubMed PubMed Citation Articles by Kimura, H. Articles by Sato, Y. Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted July 23, 2008 Accepted January 27, 2009 Distinctive localization and opposed roles of vasohibin-1 and vasohibin-2 in the regulation of angiogenesis Hiroshi Kimura, Hiroki Miyashita, Yasuhiro Suzuki, Miho Kobayashi, Kazuhide Watanabe, Hikaru Sonoda, Hideki Ohta, Takashi Fujiwara, Tooru Shimosegawa, and Yasufumi Sato* Department of Vascular Biology, Institute of Development, Aging, and Cancer, Tohoku University, Sendai, Japan Discovery Research Laboratories, Shionogi & Co., Ltd., Osaka, Japan Department of Biological Resources, INCS, Ehime University, Shitsukawa, Toon, Ehime, Japan Department of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai, Japan * Corresponding author; email: y-sato{at}idac.tohoku.ac.jp. We recently isolated a novel angiogenesis inhibitor, vasohibin-1 and its homologue vasohibin-2. In this study we characterize the role of these 2 molecules in the regulation of angiogenesis. In a mouse model of subcutaneous angiogenesis, the expression of endogenous vasohibin-1 was low in proliferating ECs at the sprouting front, but high in non-proliferating ECs in the termination zone. In contrast, endogenous vasohibin-2 was preferentially expressed in mononuclear cells mobilized from bone marrow that infiltrated the sprouting front. When applied exogenously, vasohibin-1 inhibited angiogenesis at the sprouting front where endogenous vasohibin-1 was scarce, but did not influence vascularity in the termination zone where endogenous vasohibin-1 was enriched. Exogenous vasohibin-2 prevented the termination of angiogenesis in the termination zone and increased vascularity in this region. Angiogenesis was persistent in the termination zone in the vasohibin-1 knockout mice, whereas angiogenesis was deficient at the sprouting front in the vasohibin-2 knockout mice. Supplementation of deficient proteins normalized the abnormal patterns of angiogenesis in the vasohibin knockout mice. These results indicate that vasohibin-1 is expressed in ECs in the termination zone to halt angiogenesis, whereas vasohibin-2 is expressed in infiltrating MNCs in the sprouting front to promote angiogenesis. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: T. Nasu, Y. Maeshima, M. Kinomura, K. Hirokoshi-Kawahara, K. Tanabe, H. Sugiyama, H. Sonoda, Y. Sato, and H. Makino Vasohibin-1, a Negative Feedback Regulator of Angiogenesis, Ameliorates Renal Alterations in a Mouse Model of Diabetic Nephropathy Diabetes, October 1, 2009; 58(10): 2365 - 2375. [Abstract] [Full Text] [PDF]

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