Role of platelet glycoprotein IIb/IIIa in ADP‐activated platelet adhesion to aortic endothelial cells in vitro: observation with video‐enhanced contrast microscopy
Affiliations: Department of Neurology, Keio University School of Medicine, Shinanomachi, Shinjuku‐ku, Tokyo, Japan
Note: [] Corresponding author: Yutaka Tomita, Department of Neurology, Keio University School of Medicine, Shinanomachi 35, Shinjuku‐ku, Tokyo, Japan. Tel: +81 3 3353 1211, ext 62316; Fax: +81 3 3353 1272; E‐mail: y‐[email protected].
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.
Keywords: ADP, platelet, endothelial cell, VEC microscopy, adhesion, GP IIb/IIIa
