Intracellular signal transduction and phospholipid metabolism in platelets and neutrophils

我们在本次研究支持期间的新发现如下。1.在凝血酶或A23187刺激前激活蛋白激酶C可促进血小板膜花生四烯酸的释放。2.消炎痛抑制花生四烯酸向磷脂酰乙醇胺的转移和花生四烯酸的释放。3.A23187或凝血酶可刺激血小板蛋白酪氨酸磷酸化。4.凝血酶诱导的蛋白酪氨酸磷酸化不依赖于GTP结合蛋白、细胞内外Ca~(2+)、纤维蛋白原与GPl11a的结合、血栓素A_2的形成和ADP的释放。5.A23187或血栓素A_2通过增加细胞内Ca~(2+)~(2+)~(2+)引起血小板蛋白酪氨酸磷酸化，其机制未知。6.A23187诱导的蛋白酪氨酸磷酸化可能参与了血小板聚集，但不参与分泌。7.细胞内Ca~(2+)~(2+)&Gt~(2+)与蛋白激酶C之间可能存在蛋白酪氨酸磷酸化的协同作用。

Our new findings during this research support are as follows. 1. Activation of protein kinase C before stimulation of thrombin or A23187 enhances release of arachidonate from platelet membrane. 2. Indomethacin inhibits transfer of arachidonate into phosphatidyl-ethanolamine as well as arachidonate release. 3. A23187 or thrombin can stimulate protein-tyrosine phosphorylation of platelets. 4. Thrombin-induced protein-tyrosine phosphorylation is not dependent on GTP-binding protein, intra-and extra-cellular Ca^<2+>, binding of fibrinogen to GPllbllla, thromboxane A_2 formation and released ADP. 5. A23187 or thromboxane A_2 evokes protein-tyrosin phosphorylation of platelets through increase of intracellular Ca^<2+> via unknown mechanisms. 6. A23187-induced protein-tyrosine phosphorylation may be involved in platelet aggregation but not in secretion. 7. There may be synergistic stimulation of protein-tyrosine phosphorylation between intracellular Ca^<2+> and protein kinase C.