内毒素诱导血小板20kD蛋白磷酸化、钙转运及纤维蛋白原受体显露

本文观察了E.Coli大肠杆菌内毒素对人血小板蛋白磷酸化,钙转运及纤维蛋白原受体的影响,实验采用SDS-凝胶电泳及放射自显影技术分离血小板蛋白并测定其磷酸化程度,结果发现内毒素刺激血小板后,内源性20kD蛋白迅速磷酸化,这一作用在细胞外Ca~(2 )存在时明显加强。同时还观察到血小板对~(45)Ca~(2 )摄取加强,胞浆游离Ca~(2 )升高,血小板结合荧光标记纤维蛋白原的阳性细胞百分率明显提高。提示:内毒素可能通过诱导Ca~(2 )动员,蛋白磷酸化,使血小板纤维蛋白原受体显露,导致血小板聚集。

Endotoxin induces phosphorylation of 20kD protein Ca~(2 ) transportation and fibrinogen receptor exposure in human platelets

The effects of endotoxin on protein phosphorylation, calcium transportationand fibrinogen receptor exposure in human platelets were studied. The proteins from ~(32)P-labled human platelets were separated by SDS-polyacrylamide gel electroporesis, then theprotein phosphorylation were observed with autoradiographic method. The result showedthat endotoxin rapidly induced phosphorylation of 20kD protein. An enhanced phosphory-lation of 20kD protein was seen in the presence of extracellular Ca~(2 ). Meanwhile, endo-toxin induced an increase of the cytoplasmic free Ca~(2 ) concentration and promoted ~(45)Ca_(2 )uptake by platelets. In addition, the platelets to which FITC-labled fibrinogen was boundhad increased. It suggested that the mechanism of endotoxin induced platelet aggregationinvolved in Ca~(2 ) mobilization and protein phosphorylation, which caused the fibrinogenreceptor exposure.