Endogenous Inhibitory Mechanisms and the Regulation of Platelet Function
Endogenous Inhibitory Mechanisms and the Regulation of Platelet Function
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DOI：
10.1007/978-1-61779-307-3_23
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发表时间：
2012-01-01
期刊：
影响因子：
--
通讯作者：
Jackson, Denise E.
中科院分区：
文献类型：
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作者：
Jones, Chris I.;Barrett, Natasha E.;Jackson, Denise E.
血小板对周围环境变化的反应总是激活和抑制信号之间的平衡，其累积效应是激活或静止。自由流动的血液中的血小板及其对止血和血栓形成的调节也是如此。在这篇综述中，我们认为内源性抑制机制，联合收割机，以调节血小板活化。这些包括那些来自内皮细胞（一氧化氮，前列环素，CD 39），血小板表面的抑制性受体（血小板内皮细胞粘附分子-1，癌胚抗原细胞粘附分子1，G6 b-B-包括Ig-ITIM超家族成员在ITAM相关GPVI血小板胶原相互作用和GPCR的负调节中的作用的证据-介导的信号传导和“外-内”整合素α（IIb）β（3）介导的信号传导的正调节），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）和新出现的抑制途径（经典Wnt信号传导、脑信号蛋白3A、内皮细胞特异性粘附分子和连接粘附分子-A）。
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, CD 39), 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 alpha(IIb)beta(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).