Jones Chris I, Barrett Natasha E, Moraes Leonardo A, Gibbins Jonathan M, Jackson Denise E
Institute for Cardiovascular and Metabolic Research, School of Biological Sciences, The University of Reading, Reading, UK.
Methods Mol Biol. 2012;788:341-66. doi: 10.1007/978-1-61779-307-3_23.
The response of platelets to changes in the immediate environment is always a balance between activatory and inhibitory signals, the cumulative effect of which is either activation or quiescence. This is true of platelets in free flowing blood and of their regulation of haemostasis and thrombosis. In this review, we consider the endogenous inhibitory mechanisms that combine to regulate platelet activation. These include those derived from the endothelium (nitric oxide, prostacyclin, CD39), inhibitory receptors on the surface of platelets (platelet endothelial cell adhesion molecule-1, carcinoembryonic antigen cell adhesion molecule 1, G6b-B - including evidence for the role of Ig-ITIM superfamily members in the negative regulation of ITAM-associated GPVI platelet-collagen interactions and GPCR-mediated signalling and in positive regulation of "outside-in" integrin α(IIb)β(3)-mediated signalling), intracellular inhibitory receptors (retinoic X receptor, glucocorticoid receptor, peroxisome proliferator-activated receptors, liver X receptor), and emerging inhibitory pathways (canonical Wnt signalling, Semaphorin 3A, endothelial cell specific adhesion molecule, and junctional adhesion molecule-A).
血小板对紧邻环境变化的反应始终是激活信号与抑制信号之间的一种平衡，其累积效应要么是激活，要么是静止。对于自由流动血液中的血小板及其对止血和血栓形成的调节而言都是如此。在本综述中，我们探讨了共同调节血小板激活的内源性抑制机制。这些机制包括源自内皮的机制（一氧化氮、前列环素、CD39）、血小板表面的抑制性受体（血小板内皮细胞黏附分子-1、癌胚抗原细胞黏附分子1、G6b-B——包括免疫球蛋白免疫受体酪氨酸抑制基序（Ig-ITIM）超家族成员在与免疫受体酪氨酸激活基序（ITAM）相关的糖蛋白VI（GPVI）血小板-胶原相互作用及G蛋白偶联受体（GPCR）介导的信号传导的负调节中以及在“外向内”整合素α(IIb)β(3)介导的信号传导的正调节中的作用证据）、细胞内抑制性受体（视黄酸X受体、糖皮质激素受体、过氧化物酶体增殖物激活受体、肝X受体）以及新出现的抑制途径（经典Wnt信号传导、信号素3A、内皮细胞特异性黏附分子和连接黏附分子-A）。
