Lapetina E G, Billah M M, Cuatrecasas P
Nature. 1981 Jul 23;292(5821):367-9. doi: 10.1038/292367a0.
An increase in the metabolism of phosphatidylinositol occurs in a wide variety of tissues by the action of specific ligands. In platelets, the interaction of thrombin with its receptor initiates the degradation of phosphatidylinositol by the action of a specific phospholipase C (refs 4–8). In normal conditions of stimulation, the resultant 1,2-diacylglycerol is rapidly and completely phosphorylated to phosphatidic acid. The formation of phosphatidic acid precedes the release of arachidonic acid from the phospholipids of stimulated platelets. This early appearence of phosphatidate might result in the initial production of arachidonic acid and lysophosphatidic acid by the action of a phospholipase A specific for phosphatidate. Phosphatidate/lysophosphatidate could induce calciumgating and subsequently stimulate phospholipases of the A-type, that degrade phosphatidylcholine, phosphatidyl-ethanolamine and a further fraction of phosphatidylinositol. Alternatively, the lysophosphatidate produced may serve as a substrate for the transfer of arachidonate directly from other phospholipids to form new phosphatidate which in turn can release more arachidonate. Overall, such a sequence would be equivalent to phospholipase A activation of other phospholipids. Our present data indicate that when the release of arachidonic acid is completely inhibited by cyclic AMP or quinacrine, phosphatidic acid is redirected entirely to phosphatidylinositol and there is no production of arachidonate. In these conditions, the availability of calcium might be profoundly restricted. The correlation in platelets of a phosphatidylinositol by a specific phospholipase A might suggest that these phenomena are applicable to activations in other cell systems.
在多种组织中，特定配体的作用会使磷脂酰肌醇的代谢增加。在血小板中，凝血酶与其受体的相互作用通过特定磷脂酶C的作用引发磷脂酰肌醇的降解（参考文献4 - 8）。在正常刺激条件下，生成的1,2 - 二酰基甘油会迅速且完全磷酸化为磷脂酸。磷脂酸的形成先于花生四烯酸从受刺激血小板的磷脂中释放。磷脂酸的这种早期出现可能是由于一种对磷脂酸特异的磷脂酶A的作用，导致花生四烯酸和溶血磷脂酸的初始产生。磷脂酸/溶血磷脂酸可诱导钙通道开启，随后刺激A类磷脂酶，后者降解磷脂酰胆碱、磷脂酰乙醇胺以及另一部分磷脂酰肌醇。或者，产生的溶血磷脂酸可作为底物，使花生四烯酸直接从其他磷脂转移过来形成新的磷脂酸，进而释放更多花生四烯酸。总体而言，这样的序列等同于其他磷脂的磷脂酶A激活。我们目前的数据表明，当花生四烯酸的释放被环磷酸腺苷或奎纳克林完全抑制时，磷脂酸会完全重新导向磷脂酰肌醇，且不会产生花生四烯酸。在这些条件下，钙的可用性可能会受到严重限制。血小板中特定磷脂酶A对磷脂酰肌醇的作用之间的相关性可能表明，这些现象适用于其他细胞系统的激活。
