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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Regulation of platelet granule exocytosis by S-nitrosylation
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Regulation of platelet granule exocytosis by S-nitrosylation

机译:S-亚硝基化对血小板颗粒胞吐作用的调节

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摘要

Nitric oxide (NO) regulates platelet activation by cGMP-dependent mechanisms and by mechanisms that are not completely defined. Platelet activation includes exocytosis of platelet granules, releasing mediators that regulate interactions between platelets, leukocytes, and endothelial cells. Exocytosis is mediated in part by N-ethylmaleimide-sensitive factor (NSF), an ATPase that disassembles complexes of soluble NSF attachment protein receptors. We now demonstrate that NO inhibits exocytosis of dense granules, lysosomal granules, and α-granules from human platelets by S-nitrosylation of NSF. Platelets lacking endothelial NO synthase show increased rolling on venules, increased thrombosis in arte-rioles, and increased exocytosis in vivo. Regulation of exocytosis is thus a mechanism by which NO regulates thrombosis.
机译:一氧化氮(NO)通过cGMP依赖性机制和尚未完全定义的机制来调节血小板活化。血小板活化包括血小板颗粒的胞吐作用,释放调节血小板,白细胞和内皮细胞之间相互作用的介体。胞吐作用部分由N-乙基马来酰亚胺敏感因子(NSF)介导,NSF是一种可分解​​可溶性NSF附着蛋白受体复合物的ATPase。现在,我们证明NO可以通过NSF的S-亚硝基化作用抑制人血小板中的致密颗粒,溶酶体颗粒和α-颗粒的胞吐作用。缺乏内皮一氧化氮合酶的血小板在小静脉上的滚动增加,在动脉内的血栓形成增加,并且体内胞吐增加。因此,胞吐作用的调节是NO调节血栓形成的机制。

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