Benz Peter M, Fleming Ingrid
Institute for Vascular Signalling, Centre for Molecular Medicine, Johann Wolfgang Goethe University, Frankfurt, Germany.
DZHK (German Centre for Cardiovascular Research) partner site Rhine-Main, 60590, Frankfurt am Main, Germany.
Cell Commun Signal. 2016 Sep 17;14(1):22. doi: 10.1186/s12964-016-0145-y.
Under physiological conditions, endothelial cells and the endothelial nitric oxide (NO) synthase (eNOS) are the main source of NO in the cardiovascular system. However, several other cell types have also been implicated in the NO-dependent regulation of cell function, including erythrocytes. NO derived from red blood cells has been proposed to regulate erythrocyte membrane fluidity, inhibit platelet activation and induce vasodilation in hypoxic areas, but these proposals are highly controversial. In the current issue of Cell Communication and Signaling, an elegant study by Gambaryan et al., assayed NO production by erythrocytes by monitoring the activation of the platelet intracellular NO receptor, soluble guanylyl cyclase, and its downstream kinase protein kinase G. After systematically testing different combinations of erythrocyte/platelet suspensions, the authors found no evidence for platelet soluble guanylyl cyclase/protein kinase G activation by erythrocytes and conclude that erythrocytes do not release biologically active NO to inhibit platelet activation.
在生理条件下，内皮细胞和内皮型一氧化氮合酶（eNOS）是心血管系统中一氧化氮（NO）的主要来源。然而，包括红细胞在内的其他几种细胞类型也参与了细胞功能的NO依赖性调节。有人提出红细胞衍生的NO可调节红细胞膜流动性、抑制血小板活化并在缺氧区域诱导血管舒张，但这些说法极具争议性。在本期《细胞通讯与信号传导》中，甘巴里扬等人进行了一项出色的研究，通过监测血小板细胞内NO受体、可溶性鸟苷酸环化酶及其下游激酶蛋白激酶G的激活来检测红细胞产生的NO。在系统测试不同组合的红细胞/血小板悬浮液后，作者没有发现红细胞激活血小板可溶性鸟苷酸环化酶/蛋白激酶G的证据，并得出结论：红细胞不会释放具有生物活性的NO来抑制血小板活化。
