SEARCH:   Advanced

Blood, 15 March 2004, Vol. 103, No. 6, pp. 2105-2113. Prepublished online as a Blood First Edition Paper on November 20, 2003; DOI 10.1182/blood-2003-07-2483. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-07-2483v1 103/6/2105    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 Chung, C.-H. Articles by Huang, T.-F. Search for Related Content PubMed PubMed Citation Articles by Chung, C.-H. Articles by Huang, T.-F. Related Collections Hemostasis, Thrombosis, and Vascular Biology Cell Adhesion and Motility Signal Transduction Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Aggretin, a snake venom–derived endothelial integrin 21 agonist, induces angiogenesis via expression of vascular endothelial growth factor Ching-Hu Chung, Wen-Bin Wu, and Tur-Fu Huang From the Department of Pharmacology, College of Medicine, National Taiwan University, Taipei, Taiwan. Aggretin, a collagen-like 21 agonist purified from Calloselasma rhodostoma venom, was shown to increase human umbilical vein endothelial cell (HUVEC) proliferation and HUVEC migration toward immobilized aggretin was also increased. These effects were blocked by A2-IIE10, an antibody raised against integrin 2. Aggretin bound to HUVECs in a dose-dependent and saturable manner, which was specifically inhibited by A2-IIE10, as examined by flow cytometry. Aggretin elicited significant angiogenic effects in both in vivo and in vitro angiogenesis assays, and incubation of HUVECs with aggretin activated phosphatidylinositol 3-kinase (PI3K), Akt, and extracellular-regulated kinase 1/2 (ERK1/2); these effects were blocked by A2-IIE10 or vascular endothelial growth factor (VEGF) monoclonal antibody (mAb). The angiogenic effect induced by aggretin may be via the production of VEGF because the VEGF level was elevated and VEGF mAb pretreatment inhibited Akt/ERK1/2 activation as well as the in vivo angiogenesis induced by aggretin. The VEGF production induced by aggretin can be blocked by A2-IIE10 mAb pretreatment. In conclusion, aggretin induces endothelial cell proliferation, migration, and angiogenesis by interacting with integrin 21, leading to activation of PI3K, Akt, and ERK1/2 pathways, and the increased expression of VEGF may be responsible for its angiogenic activity. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: D. Sun and K. R. McCrae Endothelial-cell apoptosis induced by cleaved high-molecular-weight kininogen (HKa) is matrix dependent and requires the generation of reactive oxygen species Blood, June 15, 2006; 107(12): 4714 - 4720. [Abstract] [Full Text] [PDF] K. Suzuki-Inoue, G. L. J. Fuller, A. Garcia, J. A. Eble, S. Pohlmann, O. Inoue, T. K. Gartner, S. C. Hughan, A. C. Pearce, G. D. Laing, et al. A novel Syk-dependent mechanism of platelet activation by the C-type lectin receptor CLEC-2 Blood, January 15, 2006; 107(2): 542 - 549. [Abstract] [Full Text] [PDF]

	Copyright © 2004 by American Society of Hematology         Online ISSN: 1528-0020