Moroi M, Okuma M, Jung S M
Department of Protein Biochemistry, Kurume University, Japan.
Biochim Biophys Acta. 1992 Oct 6;1137(1):1-9. doi: 10.1016/0167-4889(92)90092-p.
The mechanisms of platelet adhesion to collagen type III-coated wells and Matrigel-coated wells were analyzed. The adhesion of 51Cr-labeled platelets to collagen-coated wells showed a biphasic pattern. The early stage of adhesion was inhibited by antibodies against platelet glycoprotein(GP)s Ia/IIa and VI. The later stage of platelet adhesion was inhibited by an antibody against the GPIIb/IIIa complex and a concomitant release of 14C-labeled serotonin was observed. The percentage of adhered platelets was increased when a higher platelet concentration was added in the reaction medium. These results indicated that the adhesion assay of platelets to collagen-coated wells was composed of two reactions: the first one is the platelet-collagen interaction that depends on GPIa/IIa and GPVI on the platelet surface; and the second reaction is the platelet-platelet interaction, platelet aggregation, which depends on GPIIb/IIIa. The adhesion of platelets to Matrigel-coated wells was indicated to involve platelet-Matrigel interactions that were partly dependent on the laminin in the Matrigel solution.
分析了血小板与III型胶原包被孔和基质胶包被孔黏附的机制。51Cr标记的血小板与胶原包被孔的黏附呈现双相模式。黏附的早期阶段可被抗血小板糖蛋白(GP)Ia/IIa和VI的抗体抑制。血小板黏附的后期阶段可被抗GPIIb/IIIa复合物的抗体抑制,并且观察到14C标记的5-羟色胺伴随释放。当在反应介质中加入更高浓度的血小板时,黏附血小板的百分比增加。这些结果表明,血小板与胶原包被孔的黏附试验由两个反应组成:第一个是血小板-胶原相互作用,其依赖于血小板表面的GPIa/IIa和GPVI;第二个反应是血小板-血小板相互作用,即血小板聚集,其依赖于GPIIb/IIIa。血小板与基质胶包被孔的黏附表明涉及血小板-基质胶相互作用,其部分依赖于基质胶溶液中的层粘连蛋白。