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Prepublished online as a Blood First Edition Paper on July 31, 2003; DOI 10.1182/blood-2003-04-1323.

Submitted April 28, 2003
Accepted July 23, 2003
The contributions of the 2 1 integrin to vascular thrombosis in vivo
Li He, Loretta K Pappan, David G Grenache, Zhengzhi Li, Douglas M Tollefsen, Samuel A Santoro, and Mary M Zutter*
Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA
Department of Pathology & Immunology, Washington University School of Medicine, St. Louis, MO, USA
Department of Pathology & Immunology, Washington University School of Medicine, St. Louis, MO, USA; Department of Medicine, Washington University School of Medicine, St. Louis, MO, USA
* Corresponding author; email: mary.zutter{at}vanderbilt.edu.
The 2 1 integrin serves as a receptor for collagens, laminin, and/or several other nonmatrix ligands. Many studies have suggested that the 2 1 integrin is a critical mediator of platelet adhesion to collagen within the vessel wall after vascular injury and that the interactions of the platelet 2 1 integrin with subendothelial collagen after vascular injury are required for proper hemostasis. We have used the 2 1 integrin-deficient mouse to evaluate the contributions of the 2 1 integrin in two in vivo models of thrombosis. Studies using a model of endothelial injury to the carotid artery reveal that the 2 1 integrin plays a critical role in vascular thrombosis at the blood-vessel wall interface under flow conditions. In contrast, the 2 1 integrin is not required for the formation of thrombi and pulmonary emboli following intravascular injection of collagen. Our results are the first to document a critical in vivo role for the 2 1 integrin in thrombus formation at the vessel wall under conditions of shear following vascular injury.

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