Goodwin C A, Wheeler-Jones C P, Kakkar V V, Deadman J J, Authi K S, Scully M F
Thrombosis Research Institute, London, United Kingdom.
Biochem Biophys Res Commun. 1994 Jul 15;202(1):321-7. doi: 10.1006/bbrc.1994.1930.
Platelets after challenge with alpha-thrombin alone, collagen alone or thrombin/collagen mixture were observed to increase the rate of activation of prothrombin by factor Xa in the presence of factor Va and calcium ion (platelet procoagulant activity) by a maximum of 25, 45 and 110 fold, respectively. The increase in platelet procoagulant activity due to these agonists has been described previously and arises from increased expression of phosphatidylserine on the platelet surface. When platelets were treated with the thrombin receptor activating peptide (TRAP) (SFLLRNPNDKYEPK), alone or in the presence of collagen or thrombin, no change in platelet procoagulant activity was observed at concentrations of TRAP sufficient to cause increased intracellular calcium levels and protein phosphorylation in a manner similar to that of thrombin. In addition, no increase in platelet procoagulant activity was seen upon treatment with TRAP in the presence of inactivated thrombin (PPACK-thrombin). These results suggest that the thrombin-mediated increase in procoagulant activity may be due to activation of a thrombin receptor distinct from the recently cloned G-protein-coupled receptor, or to other proteolytic events on the platelet surface.
单独用α-凝血酶、单独用胶原蛋白或用凝血酶/胶原蛋白混合物刺激后的血小板，在因子Va和钙离子存在的情况下，观察到其使因子Xa激活凝血酶原的速率（血小板促凝活性）分别最多增加25倍、45倍和110倍。由于这些激动剂导致的血小板促凝活性增加此前已有描述，其源于血小板表面磷脂酰丝氨酸表达的增加。当血小板单独用凝血酶受体激活肽（TRAP）（SFLLRNPNDKYEPK）处理，或在存在胶原蛋白或凝血酶的情况下处理时，在足以引起细胞内钙水平升高和蛋白质磷酸化（类似于凝血酶作用方式）的TRAP浓度下，未观察到血小板促凝活性有变化。此外，在存在失活凝血酶（PPACK-凝血酶）的情况下用TRAP处理，也未观察到血小板促凝活性增加。这些结果表明，凝血酶介导的促凝活性增加可能是由于一种不同于最近克隆的G蛋白偶联受体的凝血酶受体被激活，或者是由于血小板表面的其他蛋白水解事件。
