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Related Collections Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, Vol. 92 No. 9 (November 1), 1998: pp. 3268-3276 Accutin, a New Disintegrin, Inhibits Angiogenesis In Vitro and In Vivo by Acting as Integrin v3 Antagonist and Inducing Apoptosis Chia Hsin Yeh, Hui-Chin Peng, and Tur-Fu Huang From the Department of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan. Endothelial integrins play an essential role in angiogenesis and cell survival. Accutin, a new member of disintegrin family derived from venom of Agkistrodon acutus, potently inhibited human platelet aggregation caused by various agonists (eg, thrombin, collagen, and, adenosine diphosphate [ADP]) through the blockade of fibrinogen binding to platelet glycoprotein IIb/IIIa (ie, integrin IIb3). In this report, we describe that accutin specifically inhibited the binding of monoclonal antibody (MoAb) 7E3, which recognizes integrin v3, to human umbilical vein endothelial cells (HUVECs), but not those of other anti-integrin MoAbs such as 21, 31, and 51. Moreover, accutin, but not the control peptide GRGES, dose-dependently inhibited the 7E3 interaction with HUVECs. Both 7E3 and GRGDS, but not GRGES or Integrelin, significantly blocked fluorescein isothiocyanate-conjugated accutin binding to HUVEC. In functional studies, accutin exhibited inhibitory effects on HUVEC adhesion to immobilized fibrinogen, fibronectin and vitronectin, and the capillary-like tube formation on Matrigel in a dose- and RGD-dependent manner. In addition, it exhibited an effective antiangiogenic effect in vivo when assayed by using the 10-day-old embryo chick CAM model. Furthermore, it potently induced HUVEC apoptotic DNA fragmentation as examined by electrophoretic and flow cytometric assays. In conclusion, accutin inhibits angiogenesis in vivo and in vitro by blocking integrin v3 of endothelial cells and by inducing apoptosis. The antiangiogenic activity of disintegrins might be explored as the target of developing the potential antimetastatic agents. © 1998 by The American Society of Hematology. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: I. Staniszewska, S. Zaveri, L. D. Valle, I. Oliva, V. L. Rothman, S. E. Croul, D. D. Roberts, D. F. Mosher, G. P. Tuszynski, and C. Marcinkiewicz Interaction of {alpha}9{beta}1 Integrin With Thrombospondin-1 Promotes Angiogenesis Circ. Res., May 11, 2007; 100(9): 1308 - 1316. [Abstract] [Full Text] [PDF] J Heidemann, D G Binion, W Domschke, and T Kucharzik Antiangiogenic therapy in human gastrointestinal malignancies. Gut, October 1, 2006; 55(10): 1497 - 1511. [Full Text] [PDF] M. S. Aguzzi, C. Giampietri, F. De Marchis, F. Padula, R. Gaeta, G. 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