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Blood, 1 December 2003, Vol. 102, No. 12, pp. 4021-4027. Prepublished online as a Blood First Edition Paper on July 31, 2003; DOI 10.1182/blood-2003-05-1391. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-05-1391v1 102/12/4021    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 Grüner, S. Articles by Nieswandt, B. Search for Related Content PubMed PubMed Citation Articles by Grüner, S. Articles by Nieswandt, B. Related Collections Hemostasis, Thrombosis, and Vascular Biology Cell Adhesion and Motility Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Multiple integrin-ligand interactions synergize in shear-resistant platelet adhesion at sites of arterial injury in vivo Sabine Grüner, Miroslava Prostredna, Valerie Schulte, Thomas Krieg, Beate Eckes, Cord Brakebusch, and Bernhard Nieswandt From the Rudolf Virchow Center for Experimental Biomedicine, University of Würzburg, Würzburg, Germany; Department of Dermatology, University of Cologne, Cologne, Germany; Department of Molecular Medicine, Max-Planck-Institute for Biochemistry, Martinsried, Germany. Damage to the integrity of the vessel wall results in exposure of the subendothelial extracellular matrix (ECM), which triggers integrin-dependent adhesion and aggregation of platelets. The role of platelet 1 integrins in these processes remains mostly undefined. Here, we demonstrate by intravital fluorescence microscopy that platelet adhesion and thrombus growth on the exposed ECM of the injured carotid artery is not significantly altered in 2-null mice and even in mice with a Cre/loxP-mediated loss of all 1 integrins on their platelets. In contrast, inhibition of IIb3 integrin on platelets in wild-type mice blocked aggregate formation and reduced platelet adhesion by 60.0%. Strikingly, IIb3 inhibition had a comparable effect in 2-null mice, demonstrating that other receptors mediate shear-resistant adhesion in the absence of functional 21 and IIb3. These were identified to be 51 and/or 61 as IIb3 inhibition abrogated platelet adhesion in 1-null mice. We conclude that shear-resistant platelet adhesion on the injured vessel wall in vivo is a highly integrated process involving multiple integrin-ligand interactions, none of which by itself is essential. 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