Engagement of Glycoprotein IIb/IIIa (α _IIb β ₃ ) on Platelets Upregulates CD40L and Triggers CD40L-Dependent Matrix Degradation by Endothelial Cells

Abstract

Platelet adhesion via GP IIb/IIIa upregulates CD40L and CD62P surface exposure. Proteolytic activity of HUVEC is induced by the concerted action of beta3-integrin-mediated platelet adhesion and subsequent CD40L-induced signals in HUVECs. Effective anti-GP IIb/IIIa or anti-CD40L strategies might, therefore, contribute to plaque stabilization.