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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2008;28:403.)
© 2008 American Heart Association, Inc.

Brief Review

Cell Adhesion Mechanisms in Platelets

David Varga-Szabo; Irina Pleines; Bernhard Nieswandt

From the Rudolf Virchow Center (D.V.-S., I.P., B.N.), DFG-Research Center for Experimental Biomedicine and the Institute of Clinical Biochemistry and Pathobiochemistry (B.N.), University of Würzburg, Germany.

Correspondence to Bernhard Nieswandt, PhD, Rudolf Virchow Center, DFG Research Center for Experimental Biomedicine, Zinklesweg 10, 97078 Würzburg, Germany. E-mail bernhard.nieswandt{at}virchow.uni.wuerzburg.de

Series Editor: Dietmar Vestweber
Vascular Adhesion Molecules
ATVB In Focus

Previous Brief Reviews in this Series:

•van Buul JD, Kanters E, and Hordijk PL. Endothelial signaling by Ig-like cell adhesion molecules. Arterioscler Thromb Vasc Biol. 2007;27:1870-1876.
•Bradfield PF, Nourshargh S, Aurrand-Lions M, Imhof BA. JAM family and related proteins in leukocyte migration. Arterioscler Thromb Vasc Biol. 2007;27:2104-2112.
•Galkina E and Ley K. Vascular adhesion molecules in atherosclerosis. Arterioscler Thromb Vasc Biol. 2007;27: 2292-2301.
•Jalkanen S, Salmi M. VAP-1 and CD73, endothelial cell surface enzymes in leukocyte extravasation. Arterioscler Thromb Vasc Biol. 2008;28:18–26.
•Vestweber, D. VE-cadharin: the major endothelial adhesion molecule controlling cellular junctions and blood vessel formation. Arterioscler Thromb Vasc Biol. 2008;28:223–232.

At sites of vascular injury, platelets come into contact with the subendothelial extracellular matrix which triggers their activation and the formation of a hemostatic plug. This process is crucial for normal hemostasis, but may also lead to pathological thrombus formation causing diseases such as myocardial infarction or stroke. The initial capture of flowing platelets is mediated by the interaction of the glycoprotein (GP) Ib-V-IX complex with von Willebrand factor (vWF) immobilized on exposed collagens. This interaction allows the binding of the collagen receptor GPVI to its ligand and to initiate cellular activation, a process that is reinforced by locally produced thrombin and soluble mediators released from platelets. These events lead to the shift of β1 and β3 integrins on the platelet surface from a low to a high affinity state, thereby enabling them to bind their ligands and to mediate firm adhesion, spreading, coagulant activity, and aggregation. This review summarizes the most important structural and functional properties of these adhesion receptors and briefly discusses their potential as targets for antithrombotic therapy.

At sites of vascular injury, platelets attach to the exposed extracellular matrix by a complex series of events involving different receptors and their signaling pathways, most notably the vWF receptor GPIb-V-IX and the collagen receptor GPVI, which induce the activation of β1 and β3 integrins and subsequent firm adhesion.

Key Words: adhesion • receptors • platelet • thrombosis • activation