Siess W, Weber P C, Lapetina E G
J Biol Chem. 1984 Jul 10;259(13):8286-92.
The present study compares the molecular mechanism by which thrombin, platelet-activating factor, and epinephrine induce platelet activation. Thrombin and platelet-activating factor induce an initial activation of phospholipase C, as measured by formation of 1,2-diacylglycerol and phosphatidic acid, during platelet shape change which is independent of and dissociated from metabolism of arachidonic acid. Phospholipase C activation and shape change are independent of extracellular Ca2+ and Mg2+. Formation of cyclooxygenase products occurs subsequent to the initial activation of phospholipase C and those metabolites are associated with platelet aggregation and further activation of phospholipase C. On the other hand, epinephrine is an unique platelet stimulus since it requires extracellular divalent cations and does not induce platelet shape change or activation of phospholipase C. Our results indicate that activation of phospholipase C may be a mechanism by which physiological agonists can activate platelets independently of extracellular divalent cations.
本研究比较了凝血酶、血小板活化因子和肾上腺素诱导血小板活化的分子机制。凝血酶和血小板活化因子在血小板形态变化过程中诱导磷脂酶C的初始活化，这可通过1,2 - 二酰甘油和磷脂酸的形成来测量，该过程独立于花生四烯酸的代谢且与之分离。磷脂酶C的活化和形态变化独立于细胞外Ca2+和Mg2+。环氧化酶产物的形成发生在磷脂酶C初始活化之后，并且这些代谢产物与血小板聚集和磷脂酶C的进一步活化相关。另一方面，肾上腺素是一种独特的血小板刺激物，因为它需要细胞外二价阳离子，且不诱导血小板形态变化或磷脂酶C的活化。我们的结果表明，磷脂酶C的活化可能是一种生理激动剂能够独立于细胞外二价阳离子激活血小板的机制。
