福斯科林
化学
蛋白激酶A
磷脂酰丝氨酸
凝血酶
血小板
卡尔帕因
血小板活化
离子载体
腺苷酸环化酶
细胞生物学
生物物理学
药理学
激酶
内科学
内分泌学
生物化学
信号转导
酶
受体
膜
生物
磷脂
医学
作者
Rong Yan,Zhicheng Wang,Ye Yuan,Hong Cheng,Kesheng Dai
标识
DOI:10.1016/j.abb.2009.02.014
摘要
The membrane microparticle (MP) formation and phosphatidylserine (PS) exposure evoked by platelet activation provide catalytic surfaces for thrombin generation. Several reports have indicated the effects of cAMP-elevating agents on agonist-induced MP formation and PS exposure; however, the mechanism still remains unclear. Here we show that inhibition of basal cyclic AMP-dependent protein kinase (PKA) activity incurred platelet MP formation and PS exposure. Pretreatment of platelets with cAMP-elevating agent, forskolin, abolished thrombin plus collagen-induced MP formation and PS exposure, and obviously decreased calcium ionophore-evoked MP shedding. Moreover, the inhibitory effects of forskolin on agonists-induced MP formation and PS exposure were reversed by the PKA inhibitor H89. PKA inhibitor-induced MP formation was dose-dependently inhibited by calpain inhibitor MDL28170, and forskolin abrogated thrombin plus collagen-induced calpain activation. In conclusion, PKA plays key roles in the regulation of platelet MP formation and PS exposure. PKA-mediated MP shedding is dependent on calpain activation.
科研通智能强力驱动
Strongly Powered by AbleSci AI