Ruan C, Tobelem G, McMichael A J, Drouet L, Legrand Y, Degos L, Kieffer N, Lee H, Caen J P
Br J Haematol. 1981 Dec;49(4):511-9. doi: 10.1111/j.1365-2141.1981.tb07259.x.
The effect on platelet function of a monoclonal platelet antibody to platelet membrane glycoprotein I was tested. This antibody, AN51, inhibited ristocetin or bovine factor VIII-induced aggregation but did not modify ADP, collagen type I or type III, thrombin or arachidonic acid induced aggregations. Furthermore, the adhesion-aggregation of platelets induced by microfibrils was also inhibited by the antibody. Platelet adhesion to rabbit aorta subendothelium was impaired by the antibody. The persistent adhesion of platelets to collagenase-treated subendothelium was also inhibited. These findings strongly suggested that platelet membrane glycoprotein I could interact with a non-collagenic microfibrillar component of subendothelium. The binding of factor VIII/von Willebrand factor to platelet membrane in the presence of ristocetin was decreased in the binding site for factor VIII/von Willebrand factor to allow platelet adhesion to subendothelium.
对一种针对血小板膜糖蛋白I的单克隆血小板抗体的血小板功能效应进行了测试。这种抗体AN51可抑制瑞斯托霉素或牛因子VIII诱导的聚集,但不改变ADP、I型或III型胶原、凝血酶或花生四烯酸诱导的聚集。此外,微原纤维诱导的血小板黏附聚集也被该抗体抑制。抗体损害了血小板对兔主动脉内皮下层的黏附。血小板对胶原酶处理的内皮下层的持续黏附也受到抑制。这些发现强烈表明,血小板膜糖蛋白I可与内皮下层的一种非胶原微原纤维成分相互作用。在存在瑞斯托霉素的情况下,因子VIII/血管性血友病因子与血小板膜的结合在因子VIII/血管性血友病因子的结合位点减少,以允许血小板黏附于内皮下层。