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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 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 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 Dubois, C. Articles by Furie, B. C. Search for Related Content PubMed PubMed Citation Articles by Dubois, C. Articles by Furie, B. C. Related Collections Cell Adhesion and Motility Signal Transduction Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY 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 From the Division of Hemostasis and Thrombosis, Center for Vascular Biology Research, Beth Israel Deaconess Medical Center; and the Department of Medicine, Harvard Medical School, Boston, MA. 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 with severe FeCl3 injury. Times to initial thrombus formation and vessel occlusion were delayed in FcR–/– compared with wild-type mice after severe injury. Platelet accumulation in wild-type mice was decreased after mild compared with 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 use 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: M. Neyman, J. Gewirtz, and M. Poncz Analysis of the spatial and temporal characteristics of platelet-delivered factor VIII-based clots Blood, August 15, 2008; 112(4): 1101 - 1108. [Abstract] [Full Text] [PDF] P. N. Bernatchez, L. Acevedo, C. Fernandez-Hernando, T. Murata, C. Chalouni, J. Kim, H. Erdjument-Bromage, V. Shah, J.-P. Gratton, E. M. McNally, et al. Myoferlin Regulates Vascular Endothelial Growth Factor Receptor-2 Stability and Function J. Biol. Chem., October 19, 2007; 282(42): 30745 - 30753. [Abstract] [Full Text] [PDF] R. J. Westrick, M. E. Winn, and D. T. Eitzman Murine Models of Vascular Thrombosis Arterioscler. Thromb. Vasc. Biol., October 1, 2007; 27(10): 2079 - 2093. 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