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Blood, 15 May 2006, Vol. 107, No. 10, pp. 3902-3906. Prepublished online as a Blood First Edition Paper on February 2, 2006; DOI 10.1182/blood-2005-09-3687. This Article Full Text (PDF) Supplemental Figures All Versions of this Article: 2005-09-3687v1 107/10/3902    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 Dubois, C. Articles by Furie, B. C Search for Related Content PubMed PubMed Citation Articles by Dubois, C. Articles by Furie, B. C Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted September 13, 2005 Accepted January 12, 2006 Glycoprotein VI-dependent and -independent pathways of thrombus formation in vivo Christophe Dubois, Laurence Panicot-Dubois, Glenn Merrill-Skoloff, Bruce Furie, and Barbara C Furie* Division of Hemostasis and Thrombosis Research, Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Boston, MA, USA; Department of Medicine, Harvard Medical School, Boston, MA, USA * Corresponding author; email: bfurie1{at}bidmc.harvard.edu. The role of the collagen receptor glycoprotein VI (GPVI) in arteriolar thrombus formation was studied in FcR null mice (FcR-/-) lacking platelet surface GPVI. Thrombi were induced with severe or mild FeCl3 injury. Collagen exposure was significantly delayed and diminished in mild compared to severe FeCl3 injury. Times to initial thrombus formation and vessel occlusion were delayed in FcR-/- compared to wild-type mice after severe injury. Platelet accumulation in wild-type mice was decreased after mild compared to severe injury. However, there was little difference between platelet accumulation after severe or mild injury in FcR-/-. These data indicate a significant role for GPVI in FeCl3-induced thrombus formation. Pretreatment of wild-type mice with lepirudin further impaired mild FeCl3-induced thrombus formation demonstrating a role for thrombin. Laser-induced thrombus formation in wild-type and FcR-/- was comparable. Collagen exposure to circulating blood was undetectable after laser injury. Normalized for thrombus size, thrombus-associated tissue factor was 5-fold higher in laser-induced thrombi than in severe FeCl3-induced thrombi. Thus, platelet activation by thrombin appears to be more important after laser injury than platelet activation by GPVI-collagen. It may thus be important when considering targets for antithrombotic therapy to employ multiple animal models with diverse pathways to thrombus formation. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: G. M. Thomas, L. Panicot-Dubois, R. Lacroix, F. Dignat-George, D. Lombardo, and C. Dubois Cancer cell-derived microparticles bearing P-selectin glycoprotein ligand 1 accelerate thrombus formation in vivo J. Exp. Med., August 31, 2009; 206(9): 1913 - 1927. [Abstract] [Full Text] [PDF] G. J. Graham, Q. Ren, J. R. Dilks, P. Blair, S. W. Whiteheart, and R. Flaumenhaft Endobrevin/VAMP-8-dependent dense granule release mediates thrombus formation in vivo Blood, July 30, 2009; 114(5): 1083 - 1090. [Abstract] [Full Text] [PDF] Y. A. Senis, M. G. Tomlinson, S. Ellison, A. Mazharian, J. Lim, Y. Zhao, K. N. Kornerup, J. M. Auger, S. G. Thomas, T. Dhanjal, et al. 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