Comfurius P, Bevers E M, Zwaal R F
Biochim Biophys Acta. 1985 Apr 26;815(1):143-8. doi: 10.1016/0005-2736(85)90485-7.
Activation of human platelets by different activators resulted in a different extent of degradation of the cytoskeletal proteins actin-binding protein and myosin, as well as of the non-cytoskeletal protein P235. The highest extent of proteolysis was observed with Ca-ionophore A23187 and decreased on going from A23187 greater than collagen plus thrombin greater than collagen greater than thrombin = ADP. The same order of potency has been found previously ((1983) Biochim. Biophys. Acta 736, 57-66) for the ability of platelet activators to induce exposure of aminophospholipids in the outer leaflet of the platelet plasma membrane, and to stimulate platelets to become procoagulant. Degradation of cytoskeletal proteins as a result of platelet stimulation by collagen plus thrombin was prevented in the presence of dibutyryl cAMP or EDTA but not in the presence of aspirin. This also runs in parallel with platelet procoagulant activity. Moreover, platelets from a patient with a partial deficiency in platelet procoagulant activity revealed a diminished extent of degradation of cytoskeletal proteins upon platelet stimulation with collagen plus thrombin. It is concluded that alterations in cytoskeletal organization upon platelet stimulation may lead to alterations in the orientation of (amino)phospholipids in the plasma membrane, and may therefore play a regulatory role in the expression of platelet procoagulant activity.
不同激活剂激活人血小板会导致细胞骨架蛋白肌动蛋白结合蛋白和肌球蛋白以及非细胞骨架蛋白P235的降解程度不同。用钙离子载体A23187时观察到的蛋白水解程度最高，从A23187开始，降解程度依次降低，顺序为：A23187＞胶原加凝血酶＞胶原＞凝血酶 = ADP。先前已发现血小板激活剂诱导血小板质膜外小叶中氨基磷脂暴露以及刺激血小板成为促凝剂的能力也具有相同的效力顺序（(1983) Biochim. Biophys. Acta 736, 57 - 66）。在存在二丁酰cAMP或EDTA的情况下，可防止胶原加凝血酶刺激血小板导致的细胞骨架蛋白降解，但在存在阿司匹林的情况下则不能。这也与血小板促凝活性平行。此外，一名血小板促凝活性部分缺乏的患者的血小板在用胶原加凝血酶刺激时，细胞骨架蛋白的降解程度降低。结论是，血小板刺激时细胞骨架组织的改变可能导致质膜中（氨基）磷脂方向的改变，因此可能在血小板促凝活性的表达中起调节作用。
