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首页> 外文期刊>Journal of Cellular Physiology >Estrogen-responsive nitroso-proteome in uterine artery endothelial cells: role of endothelial nitric oxide synthase and estrogen receptor-beta.
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Estrogen-responsive nitroso-proteome in uterine artery endothelial cells: role of endothelial nitric oxide synthase and estrogen receptor-beta.

机译：过量nitroso-proteome在子宫动脉内皮细胞,内皮细胞的作用一氧化氮合酶,雌激素receptor-beta。

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Covalent adduction of a NO moiety to cysteines (S-nitrosylation or SNO) is a major route for NO to directly regulate protein functions. In uterine artery endothelial cells (UAEC), estradiol-17beta (E2) rapidly stimulated protein SNO that maximized within 10-30 min post-E2 exposure. E2-bovine serum albumin stimulated protein SNO similarly. Stimulation of SNO by both was blocked by ICI 182, 780, implicating mechanisms linked to specific estrogen receptors (ERs) localized on the plasma membrane. E2-induced protein SNO was attenuated by selective ERbeta, but not ERalpha, antagonists. A specific ERbeta but not ERalpha agonist was able to induce protein SNO. Overexpression of ERbeta, but not ERalpha, significantly enhanced E2-induced SNO. Overexpression of both ERs increased basal SNO, but did not further enhance E2-stimulated SNO. E2-induced SNO was inhibited by N-nitro-L-arginine-methylester and specific endothelial NO synthase (eNOS) siRNA. Thus, estrogen-induced SNO is mediated by endogenous NO via eNOS and mainly ERbeta in UAEC. We further analyzed the nitroso-proteomes by CyDye switch technique combined with two-dimensional (2D) fluorescence difference gel electrophoresis. Numerous nitrosoprotein (spots) were visible on the 2D gel. Sixty spots were chosen and subjected to matrix-assisted laser desorption/ionization-time of flight mass spectrometry. Among the 54 identified, nine were novel SNO-proteins, 32 were increased, eight were decreased, and the rest were unchanged by E2. Tandom MS identified Cys139 as a specific site for SNO in GAPDH. Pathway analysis of basal and estrogen-responsive nitroso-proteomes suggested that SNO regulates diverse protein functions, directly implicating SNO as a novel mechanism for estrogen to regulate uterine endothelial function and thus uterine vasodilatation.
机译：共价内收的没有半胱氨酸的一部分(S-nitrosylation或SNO)是一个主要的途径直接调节蛋白质的功能。子宫动脉内皮细胞(06),estradiol-17beta (E2)迅速刺激蛋白质在10 ~ 30分钟post-E2 SNO,最大化曝光。蛋白质SNO类似。182年被ICI, 780,暗示机制与特定的雌激素受体在质膜(ERs)本地化。E2-induced蛋白质SNO减毒了选择性ERbeta,但不是ERalpha拮抗剂。具体ERbeta但不是ERalpha受体激动剂可以诱导蛋白质SNO。但不是ERalpha,显著增强E2-induced SNO。增加基底SNO,但没有进一步加强E2-stimulated SNO。由N-nitro-L-arginine-methylester和具体内皮没有合酶(以挪士)核。雌激素使SNO由内生不主要通过以挪士和ERbeta 06。分析了nitroso-proteomes CyDye开关结合二维(2 d)的技术荧光差异凝胶电泳。众多nitrosoprotein(点)是可见的二维凝胶。matrix-assisted激光解吸/电离时间飞行质量谱分析。小说SNO-proteins 32增加8E2下降,其余没有变化。Tandom确定Cys139女士作为一个特定的网站在GAPDH SNO。过量nitroso-proteomes建议SNO调节不同蛋白质的功能,直接暗示SNO作为小说的机制雌激素对子宫内皮功能因此子宫血管舒张。

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