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Thrombin and Platelet Activation*

Lawrence F. Brass, MD, PhD
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*From the Departments of Medicine and Pharmacology, and the Center for Experimental Therapeutics, University of Pennsylvania, PA.

Correspondence to: Lawrence F. Brass, MD, PhD, University of Pennsylvania, Room 915 BRB-II, 421 Curie Blvd, Philadelphia, PA 19104; e-mail: Brass@mail.med.upenn.edu



Chest. 2003;124(3_suppl):18S-25S. doi:10.1378/chest.124.3_suppl.18S
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The accumulation of thrombin at sites of vascular injury provides one of the chief means for recruiting platelets into a growing hemostatic plug. Studies completed over the past 10 years show that platelet responses to thrombin are mediated by a subset of G protein-coupled receptors known as protease-activated receptors. These receptors are activated on cleavage by thrombin, initiating the intracellular signaling events needed to transform mobile, nonadhesive platelets into cells that can participate in the growth of an immobile hemostatic plug. How this is accomplished is the subject of this review.

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