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J. Biol. Chem., Vol. 280, Issue 28, 26002-26010, July 15, 2005

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Differential Involvement of ERK2 and p38 in Platelet Adhesion to Collagen^*

Alexandra Mazharian, Séverine Roger, Pascal Maurice¶, Eliane Berrou, Michel R. Popoff||, Marc F. Hoylaerts**, Françoise Fauvel-Lafeve¶, Arnaud Bonnefoy¶, and Marijke Bryckaert

From the Hôpital Lariboisière, U689 INSERM, IFR139, 8 rue Guy Patin, Paris 75010, France, ^¶Hôpital Saint Louis, U553 INSERM, IFR105 Hôpital Saint Louis, 75010 Paris, France, ^||Institut Pasteur, Paris 75724 Paris Cedex 15, France, and ^**Center for Molecular and Vascular Biology, University of Leuven, 3000 Leuven, Belgium

We investigated the role of two MAP kinases, ERK2 and p38, in platelet adhesion and spreading over collagen matrix in static and blood flow conditions. P38 was involved in collagen-induced platelet adhesion and spreading in static adhesion conditions, whereas ERK2 was not. In blood flow conditions, with shear rates of 300 or 1500 s^–1, ERK2 and p38 displayed differential involvement in platelet adhesion, depending on the presence or absence of the von Willebrand factor (vWF). Low collagen coverage densities (0.04 µg/cm²) did not support vWF binding. During perfusions over this surface, platelet adhesion was not affected by the inhibition of ERK2 phosphorylation by PD 98059. However, abolishing p38 activation by SB 203580 treatment reduced platelet adhesion by 67 ± 9% at 300 s^–1 and 56 ± 2% at 1500 s^–1. In these conditions, the p38 activity required for platelet adhesion depends on the 21 collagen receptor. At higher collagen coverage densities (0.8 µg/cm²) supporting vWF binding, the inhibition of ERK2 activity by PD 98059 decreased adhesion by 47 ± 6% at 300 s^–1 and 72 ± 3% at 1500 s^–1, whereas p38 inhibition had only a small effect. The ERK2 activity required for platelet adhesion was dependent on the interaction of vWF with GPIb. In conclusion, ERK2 and p38 have complementary effects in the control of platelet adhesion to collagen in a shear stress-dependent manner.

Received for publication, December 15, 2004 , and in revised form, April 25, 2005.

^* This work was supported by the Association pour la Recherche sur le Cancer (ARC Contract 5820) and the Simone and Cino del Duca Foundation. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Both authors contributed equally to this work.

To whom correspondence should be addressed: Hôpital Lariboisière, U689-E6 INSERM, 8 rue Guy Patin, Paris 75010, France. Tel.: 33-1-53-20-37-80; Fax: 33-1-49-95-85-79; E-mail: marijke.bryckaert{at}larib.inserm.fr.

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