Pulcinelli F M, Ashby B, Gazzaniga P P, Daniel J L
Department of Experimental Medicine and Pathology, University La Sapienza, Rome, Italy.
FEBS Lett. 1995 May 1;364(1):87-90. doi: 10.1016/0014-5793(95)00352-a.
A selective inhibitor of protein kinase C (PKC), Ro 31-8220, blocks pleckstrin (P47) phosphorylation in platelets activated with either ADP, ADP plus synthetic thromboxane agonist U46619 and ADP plus U46619 plus epinephrine, while inducing a weak inhibition of platelet aggregation, and no significant effect on the fibrinogen binding. In platelets activated by U46619 alone, P47 phosphorylation, platelet aggregation, fibrinogen binding and serotonin release are all inhibited by Ro 31-8220. In the presence of an ADP scavenger system, U46619 induces pleckstrin phosphorylation, serotonin release and calcium mobilization but not platelet aggregation and fibrinogen binding, unless epinephrine is added.
(1) PKC activation is required for ADP secretion; (2) ADP or epinephrine are essential for fibrinogen receptor exposure induced by U46619; (3) fibrinogen receptor exposure induced by ADP is independent of activation of PKC.
蛋白激酶C（PKC）的选择性抑制剂Ro 31-8220可阻断用二磷酸腺苷（ADP）、ADP加合成血栓素激动剂U46619以及ADP加U46619加肾上腺素激活的血小板中的普列克底物蛋白（P47）磷酸化，同时对血小板聚集产生微弱抑制作用，且对纤维蛋白原结合无显著影响。在仅由U46619激活的血小板中，P47磷酸化、血小板聚集、纤维蛋白原结合和5-羟色胺释放均受到Ro 31-8220的抑制。在存在ADP清除系统的情况下，U46619可诱导普列克底物蛋白磷酸化、5-羟色胺释放和钙动员，但不会诱导血小板聚集和纤维蛋白原结合，除非添加肾上腺素。
（1）ADP分泌需要PKC激活；（2）ADP或肾上腺素对于U46619诱导的纤维蛋白原受体暴露至关重要；（3）ADP诱导的纤维蛋白原受体暴露独立于PKC激活。
