磷酸化ERK1/2对大鼠体外血小板聚集的可能作用  

Effect of ERK1/2 phosphorylation on the aggregation of the rat platelets in vitro

作　　者：刘玉玲[1] 芦玲巧[1] 张立克[1] 姚兴海[1] 

机构地区：[1]首都医科大学病理生理教研室,北京100054

出　　处：《中国病理生理杂志》2005年第1期113-115,共3页Chinese Journal of Pathophysiology

基　　金：北京市教委基金资助项目(No.99KJ15)

摘　　要：目的观察两种激动剂诱导下,MEK1/2抑制剂PD098059对大鼠体外血小板聚集及磷酸化ERK1/2的影响。方法采用比浊法测定血小板最大聚集率,并观察最大聚集率发生时间,以及PD098059对血小板聚集的抑制率;采用Westernblot测定ERK1/2磷酸化表达。结果凝血酶和ADP均可诱导血小板聚集及ERK1/2磷酸化的表达;PD098059ADP降低血小板最大聚集率及ERK1/2磷酸化表达;凝血酶与ADP诱导的血小板最大聚集率、最大聚集率发生时间及对PDO98059的反应均有差异。结论ERK1/2为血小板聚集的信号转导途径之一;但在不同激活剂引起的血小板聚集中所起的作用不尽相同。AIM: To study the influence of PD098059 on the rat platelet aggregation rate and the phosphorylation of ERK1/2 induced by the different agonists, and to observe the effects of phosphorylation of ERK1/2 on the platelet aggregation. METHODS: The maximal aggregation rate (MAR) was measured by nephelometry. The inhibitory rate of PD098059 and the appearing time of MAR were also observed. ERK1/2 phosphorylation was detected by Western blot. RESULTS: The phosphorylation of ERK1/2 was detected during aggregation induced by thrombin and ADP. PD098059 inhibited the MAR and phosphorylation of ERK1/2. Effects of PD098059 were different on the aggregation induced by thrombin and ADP. CONCLUSIONS: The phosphorylation of ERK1/2 is one of the cellular signal transduction mechanisms of platelets aggregation. Phosphorylation of ERK1/2 plays different roles during the platelet aggregation induced by thrombin and ADP. [

关 键 词：有丝分裂素激活蛋白激酶类 血小板聚集 信号转导 

分 类 号：R363[医药卫生—病理学]