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Blood, 15 March 2007, Vol. 109, No. 6, pp. 2424-2429. Prepublished online as a Blood First Edition Paper on November 21, 2006; DOI 10.1182/blood-2006-06-028241. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-06-028241v1 109/6/2424    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 Chauhan, A. K. Articles by Wagner, D. D. Search for Related Content PubMed PubMed Citation Articles by Chauhan, A. K. Articles by Wagner, D. D. 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 von Willebrand factor and factor VIII are independently required to form stable occlusive thrombi in injured veins Anil K. Chauhan1,2, Janka Kisucka1,2, Colin B. Lamb1, Wolfgang Bergmeier1,2, and Denisa D. Wagner1,2 1 CBR Institute for Biomedical Research and 2 Department of Pathology, Harvard Medical School, Boston, MA von Willebrand factor (VWF) protects factor VIII (FVIII) from proteolysis and mediates the initial contact of platelets with the injured vessel wall, thus playing an important role in hemostasis and thrombosis. VWF is crucial for the formation of occlusive thrombi at arterial shear rates. However, with only a few conflicting studies published, the role of VWF in venous thrombosis is still unclear. Using gene-targeted mice, we show that in ferric chloride–injured veins platelet adhesion to subendothelium is decreased and thrombus growth is impaired in VWF–/– mice when compared with wild type (WT). We also observed increased embolization in the VWF–/– mice, which was due to lower FVIII levels in these mice as recombinant factor VIII (r-FVIII) restored thrombus stability. Despite normalization of blood clotting time and thrombus stability after r-FVIII infusion, the VWF–/– venules did not occlude. Transgenic platelets lacking the VWF receptor GPIb extracellular domain showed decreased adhesion to injured veins. But, after a delay, all the injured venules occluded in these transgenic mice. Thus, VWF likely uses other adhesion receptors besides GPIb in thrombus growth under venous shear conditions. Our studies document crucial roles for VWF and FVIII in experimental thrombosis under venous flow conditions in vivo. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: M. N. O'Connor, I. I. Salles, A. Cvejic, N. A. Watkins, A. Walker, S. F. Garner, C. I. Jones, I. C. Macaulay, M. Steward, J.-J. Zwaginga, et al. Functional genomics in zebrafish permits rapid characterization of novel platelet membrane proteins Blood, May 7, 2009; 113(19): 4754 - 4762. [Abstract] [Full Text] [PDF] A. K. Chauhan, M. T. Walsh, G. Zhu, D. Ginsburg, D. D. Wagner, and D. G. Motto The combined roles of ADAMTS13 and VWF in murine models of TTP, endotoxemia, and thrombosis Blood, April 1, 2008; 111(7): 3452 - 3457. [Abstract] [Full Text] [PDF] A. K. Chauhan, J. Kisucka, M. R. Cozzi, M. T. Walsh, F. A. Moretti, M. Battiston, M. Mazzucato, L. De Marco, F. E. Baralle, D. D. Wagner, et al. Prothrombotic Effects of Fibronectin Isoforms Containing the EDA Domain Arterioscler. Thromb. Vasc. Biol., February 1, 2008; 28(2): 296 - 301. [Abstract] [Full Text] [PDF]

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