SEARCH:   Advanced

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 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 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 Kimura, H. Articles by Sato, Y. Search for Related Content PubMed PubMed Citation Articles by Kimura, H. Articles by Sato, Y. Related Collections Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  VASCULAR BIOLOGY Distinctive localization and opposed roles of vasohibin-1 and vasohibin-2 in the regulation of angiogenesis Hiroshi Kimura1,2, Hiroki Miyashita1, Yasuhiro Suzuki1, Miho Kobayashi1, Kazuhide Watanabe1, Hikaru Sonoda3, Hideki Ohta3, Takashi Fujiwara4, Tooru Shimosegawa2, and Yasufumi Sato1 1 Department of Vascular Biology, Institute of Development, Aging, and Cancer, Tohoku University, Sendai; 2 Department of Gastroenterology, Tohoku University Graduate School of Medicine, Sendai; 3 Discovery Research Laboratories, Shionogi and Co, Osaka; and 4 Department of Biological Resources, Integrated Center for Science (INCS), Ehime University, Shitsukawa, Ehime, Japan 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 nonproliferating endothelial cells (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 mononuclear cells 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]

	Copyright © 2009 by American Society of Hematology         Online ISSN: 1528-0020