Gerrard J M, Robinson P
Biochim Biophys Acta. 1984 Oct 4;795(3):487-92. doi: 10.1016/0005-2760(84)90177-2.
Stimulation of platelets by thrombin produced a rise in [32P]phosphatidic acid labelling of platelets which was greater in medium without added calcium than in medium with 2.5 mM calcium. A rise in [32P]lysophosphatidic acid was also seen in platelets stimulated by thrombin in the presence of 2.5 mM extracellular calcium, though it was of lesser magnitude (average 35%) than the rise in phosphatidic acid. In platelets resuspended without added calcium no change in [32P]lysophosphatidic acid was seen in response to thrombin. Lysophosphatidic acid can itself induce platelet aggregation. Similarly to the calcium ionophore A23187, lysophosphatidic acid produced minimal change (in medium with no added calcium) to no change (in medium with 2.5 mM external calcium) in [32P]lysophosphatidic acid. The endoperoxide analog U46619 produced changes in 32P-labelling of platelet phosphatidic and lysophosphatidic acid similar to those produced by thrombin but of lesser magnitude. The results of these studies show that the action of lysophosphatidic acid on platelets differs from the action of thrombin, U46619 and platelet-activating factor, which produce a rapid rise in [32P]phosphatidic acid, and suggests that lysophosphatidic acid, like A23187, largely bypasses the initial receptor-coupled breakdown of phosphoinositides leading to formation of diacylglycerols and phosphatidic acid.
凝血酶刺激血小板会使血小板的[32P]磷脂酸标记增加，在无钙添加的培养基中增加幅度大于在含有2.5 mM钙的培养基中。在存在2.5 mM细胞外钙的情况下，凝血酶刺激的血小板中[32P]溶血磷脂酸也会增加，不过其增加幅度（平均35%）小于磷脂酸的增加幅度。在无钙添加重悬的血小板中，凝血酶刺激后[32P]溶血磷脂酸未见变化。溶血磷脂酸本身可诱导血小板聚集。与钙离子载体A23187类似，溶血磷脂酸使[32P]溶血磷脂酸在无钙添加的培养基中变化极小（在含有2.5 mM细胞外钙的培养基中无变化）。内过氧化物类似物U46619使血小板磷脂酸和溶血磷脂酸的32P标记变化与凝血酶所致相似，但幅度较小。这些研究结果表明，溶血磷脂酸对血小板的作用不同于凝血酶、U46619和血小板活化因子，后三者会使[32P]磷脂酸迅速增加，这表明溶血磷脂酸与A23187一样，在很大程度上绕过了磷酸肌醇最初由受体偶联导致二酰甘油和磷脂酸形成的分解过程。
