Rittenhouse-Simmons S, Deykin D
J Clin Invest. 1977 Aug;60(2):495-8. doi: 10.1172/JCI108801.
In studies conducted with human gel-filtered platelets, we have found: (a) that the release of serotonin and transfer of [3H]arachidonic acid from phosphatidylcholine and phosphatidylinositol to plasmalogen phosphatidylethanolamine which are associated with the activation of platelets by thrombin are both strongly dependent upon the presence of metabolic ATP; (b) that serotonin release and arachidonic acid mobilization in labeled phosphatides are promoted by the calcium ionophore A-23187 in media free of calcium ions; (c) that inhibitors of ATP synthesis, while leading to impairment of the release reaction induced by ionophore, do not inhibit ionophore-stimulated mobilization of arachidonic acid. We conclude that the activation of phospholipase A2 responsible for freeing arachidonic acid from platelet phosphatides is solely dependent upon the increased cytoplasmic levels of calcium ions promoted by either ionophore or, in an energy-dependent fashion by thrombin. Phospholipase activation is not a function of latent hydrolytic activity made available by the release reaction.
在用人类凝胶过滤血小板进行的研究中,我们发现:(a) 血清素的释放以及[3H]花生四烯酸从磷脂酰胆碱和磷脂酰肌醇向缩醛磷脂酰乙醇胺的转移,这两者都与凝血酶激活血小板相关,且都强烈依赖于代谢ATP的存在;(b) 在无钙离子的介质中,钙离子载体A - 23187可促进标记磷脂中血清素的释放和花生四烯酸的动员;(c) ATP合成抑制剂虽然会导致离子载体诱导的释放反应受损,但并不抑制离子载体刺激的花生四烯酸动员。我们得出结论,负责从血小板磷脂中释放花生四烯酸的磷脂酶A2的激活仅依赖于由离子载体或以能量依赖方式由凝血酶促进的细胞质钙离子水平的升高。磷脂酶激活不是释放反应所提供的潜在水解活性的功能。