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细胞表面血小板组织因子表达:通过P2Y₁₂进行调节,并与血小板残留活性相关

Marta Brambilla¹, Alessia Becchetti¹, Gian Enrico Rovati²

¹Centro Cardiologico Monzino IRCCS, Milan, Italy (M.B., A. Becchetti, N.C., M. Conti, P.C., A. Bonomi, D.T., P.J.W., J.C., G.M., M. Camera).

Arteriosclerosis, thrombosis, and vascular biology

|August 17, 2023

概括

血小板组织因子 (TF) 暴露主要由P2Y₁₂受体调节,而不是P2Y₁. P2Y₁₂对抗剂有效降低TF阳性血小板,这对于评估抗血小板治疗患者的残留反应性至关重要.

科学领域:

血液学和血栓症研究研究
血小板生理学和功能
心血管疾病的发病源是心血管疾病的发病源.

背景情况:

腺二酸盐 (ADP) 诱导的血小板激活导致组织因子 (TF) 的细胞表面表达.
在调节血小板TF暴露方面,ADP受体P2Y₁和P2Y₁₂的特定作用仍然在很大程度上未被描述.
了解这些途径对于管理心血管疾病中血栓形成风险至关重要.

研究的目的:

研究P2Y₁和P2Y₁₂受体在血小板上ADP诱导的TF暴露中的参与.
为了评估TF阳性 (TF^pos) 血小板的调节,在接受抗P2Y₁₂治疗的冠状动脉疾病患者中.
为了阐明TF在血小板内的细胞内定位.

主要方法:

在体外分析P2Y₁或P2Y₁₂对ADP诱导的TF表达和活性的影响,使用流细胞计和血栓生成试验.
用VASP血小板反应指数测量P2Y₁₂抑制冠状动脉疾病患者 (n=238) 冠状动脉表达的实体评估,这些患者接受了用克洛皮多格雷尔,普拉苏格雷尔或提卡格雷勒治疗.
传输电子显微镜 (TEM) 和灰色血小板综合征患者的分析,以确定TF细胞内定位和释放机制.

主要成果:

P2Y₁₂抑制显著减少ADP诱导的TF^pos-血小板在体外以度依赖的方式,而P2Y₁抑制没有显著的影响.
在冠状动脉疾病患者中,P2Y₁₂抑制与ADP诱导的血小板TF表达减少相关,尽管克洛皮多格雷尔响应者的子集显示残留TF暴露.
低于20%的VASP血小板反应指数有效地识别出具有低TF^pos-血小板的患者,以及胆固醇降低了TF表达,但没有α-颗粒释放,这表明TF被存储在开放的管系统中.

结论:

血小板TF表达主要由P2Y₁₂受体调节,P2Y₁₂对手在降低TF^pos-血小板的调节方面表现出有效性.
在用克洛皮多格雷尔治疗的患者中评估TF^pos-血小板可以识别残留血小板反应的个体,即使在明显良好反应者中.
TF被存储在血小板的开放状系统中,其在激活时的膜暴露是与α-颗粒释放不同的过程.

关键词:

P2Y12对抗剂的使用.这是一个P2Y12受体.血小板是血液中的血小板.冠状动脉疾病是一种冠状动脉疾病.血栓形成蛋白质的形成.

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