Polysulfides (H(2)S(n)) produced from the interaction of hydrogen sulfide (H(2)S) and nitric oxide (NO) activate TRPA1 channels.
Polysulfides (H(2)S(n)) produced from the interaction of hydrogen sulfide (H(2)S) and nitric oxide (NO) activate TRPA1 channels.
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DOI：
10.1038/srep45995
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发表时间：
2017-04-05
影响因子：
4.6
通讯作者：
Kimura H
中科院分区：
文献类型：
--
作者：
Miyamoto R;Koike S;Takano Y;Shibuya N;Kimura Y;Hanaoka K;Urano Y;Ogasawara Y;Kimura H
硫化氢（H2S）与另一种气体信号分子一氧化氮（NO）对离子通道和血管系统具有协同作用。然而，这种协同作用的机制尚不清楚。在这里，我们发现H2S和NO之间的相互作用产生多硫化物（H2Sn），激活瞬时受体电位锚蛋白1 （TRPA1）通道。高效液相色谱串联质谱分析，以及细胞内Ca2+和H2Sn的成像显示，通过氰解和还原物质，如二硫苏糖醇（DTT）、半胱氨酸和谷胱甘肽（GSH）， H2Sn及其作用被消除。然而，H2S和NO相互作用的其他潜在产物硝基或亚硝基过硫化物的作用不受氰解或还原性物质的影响。该研究表明H2Sn是H2S和NO协同作用的产物，为研究H2S和NO的信号机制提供了新的思路。
Hydrogen sulfide (H2S) exerts synergistic effects with another gaseous signaling molecule nitric oxide (NO) on ion channels and vasculature. However, the mechanism of the synergy is not well understood. Here, we show that the interaction between H2S and NO generates polysulfides (H2Sn), which activate transient receptor potential ankyrin 1 (TRPA1) channels. High performance liquid chromatography with tandem mass spectrometry analysis, along with the imaging of intracellular Ca2+ and H2Sn, showed that H2Sn and their effects were abolished by cyanolysis and by reducing substances such as dithiothreitol (DTT), cysteine, and glutathione (GSH). However, the effects of nitroxyl or nitrosopersulfide, other potential products of H2S and NO interaction, are not affected by cyanolysis or reducing substances. This study demonstrates that H2Sn are products of synergy between H2S and NO and provides a new insight into the signaling mechanisms.