Feinstein M B, Halenda S P
Department of Pharmacology, University of Connecticut Health Center, Farmington 06032.
Experientia. 1988 Feb 15;44(2):101-4. doi: 10.1007/BF01952189.
A major route for the release of arachidonic acid from platelet phospholipids appears to be catalyzed by a phospholipase A2 that can be stimulated by a rise of cytosolic Ca2+. This paper discusses certain other mechanisms for regulation of this process. Release of arachidonic acid by calcium ionophores is potentiated by pretreatment with stimulators of protein kinase C; e.g. diglyceride, phorbol esters and the terpene diester mezerein. This effect appears to be coincident with phosphorylation of a certain group of proteins (not 47 KDa protein), and is sensitive to depletion of ATP, activation of Ca2+ dependent phosphatase, and the kinase C inhibitor H-7, but is unaffected by Na+/H+ exchange inhibitors. Recent results in other cell types strongly indicate that phospholipase A2 is also directly under control of certain GTP-binding proteins.
从血小板磷脂中释放花生四烯酸的一条主要途径似乎是由一种磷脂酶A2催化的，该磷脂酶A2可被胞质Ca2+浓度升高所刺激。本文讨论了调节这一过程的某些其他机制。用蛋白激酶C的刺激剂（如甘油二酯、佛波酯和萜烯二酯芫花酯）预处理可增强钙离子载体介导的花生四烯酸释放。这种效应似乎与某一组蛋白质（而非47 kDa蛋白质）的磷酸化同时发生，并且对ATP耗竭、Ca2+依赖性磷酸酶的激活以及激酶C抑制剂H-7敏感，但不受Na+/H+交换抑制剂的影响。其他细胞类型的最新研究结果有力地表明，磷脂酶A2也直接受某些GTP结合蛋白的控制。
