Batar P, Dale G L
W. K. Warren Medical Research Institute and the Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, 73190, USA.
J Lab Clin Med. 2001 Dec;138(6):393-402. doi: 10.1067/mlc.2001.120049.
Collagen and thrombin-activated (COAT) platelets represent a unique subset of activated platelets that exhibit high levels of several adhesive and procoagulant alpha-granule proteins on their surface. In this report we demonstrate that a similar subpopulation of platelets can also be generated by the combined stimulation of Fc gamma RIIA and thrombin receptors. Platelets activated in this manner are referred to as Fc receptor and thrombin-activated (FcRT) platelets, and they share many of the characteristics of the formerly observed COAT platelets, including aminophospholipid exposure, adhesive and procoagulant protein enrichment, increased frequency among young platelets, and sensitivity to transglutaminase inhibitors. Although Fc gamma RIIA receptor activation can be achieved either with anti-CD9 monoclonal antibodies (ALB-6 and ML-13) or with direct Fc receptor cross-linking, FcRT platelet generation occurs only with concurrent or slightly delayed thrombin stimulation. In fact, when thrombin was the second agonist, time delays of up to 120 seconds after Fc gamma RIIA receptor stimulation had little effect on the generation of FcRT platelets; however, a similar delay for convulxin plus thrombin activation results in a 90% diminution in COAT platelet production. FcRT platelet formation in platelet-poor plasma and whole blood was also investigated, and results were similar to those observed with gel-filtered platelets. Previous experiments with COAT platelet formation used physiologic agonists (collagen and thrombin) that might be encountered under either physiologic or pathologic conditions; however, the current experiments with Fc receptor stimulation offer the first example in which these highly prohemostatic platelets are likely to be strictly pathogenic.
胶原蛋白和凝血酶激活（COAT）的血小板代表了活化血小板的一个独特亚群，其表面呈现出高水平的几种粘附性和促凝血α-颗粒蛋白。在本报告中，我们证明通过FcγRIIA和凝血酶受体的联合刺激也可以产生类似的血小板亚群。以这种方式活化的血小板被称为Fc受体和凝血酶激活（FcRT）血小板，它们具有许多先前观察到的COAT血小板的特征，包括氨基磷脂暴露、粘附性和促凝血蛋白富集、年轻血小板中频率增加以及对转谷氨酰胺酶抑制剂敏感。尽管FcγRIIA受体激活可以通过抗CD9单克隆抗体（ALB-6和ML-13）或直接Fc受体交联来实现，但FcRT血小板的产生仅在同时或稍延迟的凝血酶刺激下发生。事实上，当凝血酶作为第二种激动剂时，FcγRIIA受体刺激后长达120秒的时间延迟对FcRT血小板的产生几乎没有影响；然而，convulxin加凝血酶激活的类似延迟会导致COAT血小板产生减少90%。还研究了在贫血小板血浆和全血中FcRT血小板的形成，结果与在凝胶过滤血小板中观察到的结果相似。先前关于COAT血小板形成的实验使用了生理激动剂（胶原蛋白和凝血酶），这些激动剂可能在生理或病理条件下遇到；然而，目前关于Fc受体刺激的实验提供了第一个例子，其中这些高度促止血的血小板可能严格致病。
