Role of platelet glycoprotein IIb/IIIa in ADP‐activated platelet adhesion to aortic endothelial cells in vitro: observation with video‐enhanced contrast microscopy

Abstract

Intravascular thrombus formation downstream of cerebral arterial occlusion may result in necrosis of ischemic tissue. To clarify the causative mechanisms, interaction between adenosine‐5^′‐diphosphate (ADP)‐activated platelets and cultured human aortic endothelial cells (HAEC) was examined by employing video enhanced contrast‐differential interference contrast (VEC‐DIC) microscopy. The numbers of (1) control/platelets, (2) ADP‐activated platelets, (3) ADP‐activated, anti‐platelet GP Ibα antibody (GUR20‐5)‐treated platelets, and (4) ADP‐activated, platelet GP IIb/IIIa antagonist (TAK‐029)‐treated platelets, associated with HAEC after superfusion and wash‐out were counted in visual fields of 30×30 μm². Many ADP‐activated platelets adhered to HAEC directly, while almost no platelets adhered to HAEC in the control. The adhesion was almost completely blocked by the GP IIb/IIIa antagonist, but not by GP Ibα antibody. We conclude that initial binding of ADP‐activated platelets to HAEC is mediated by platelet GP IIb/IIIa in this in vitro system.