首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Molecular mechanisms of dexamethasone inhibition of nitric oxide synthase expression in interleukin 1β-stimulated mesangial cells: Evidence for the involvement of transcriptional and posttranscriptional regulation
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Molecular mechanisms of dexamethasone inhibition of nitric oxide synthase expression in interleukin 1β-stimulated mesangial cells: Evidence for the involvement of transcriptional and posttranscriptional regulation

机译:地塞米松抑制白介素1β刺激的系膜细胞中一氧化氮合酶表达的分子机制:参与转录和转录后调控的证据。

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摘要

Inducible nitric oxide synthase (iNOS; EC 1.14.13.39) is expressed in rat glomerular mesangial cells upon exposure to the inflammatory cytokine interleukin 1β (IL-1β). We have reported that nanomolar concentrations of dexamethasone suppress IL-1β-induced iNOS protein expres- sion and production of nitrite, the stable end product of NO formation, without affecting IL-1β-triggered increase in iNOS mRNA levels. We now have studied the mechanisms by which dexamethasone suppresses IL-1β-stimulated iNOS expres- sion in mesangial cells.
机译:诱导型一氧化氮合酶(iNOS; EC 1.14.13.39)在暴露于炎性细胞因子白介素1β(IL-1β)后在大鼠肾小球系膜细胞中表达。我们已经报道,纳摩尔浓度的地塞米松抑制IL-1β诱导的iNOS蛋白表达和亚硝酸盐(NO形成的稳定终产物)的产生,而不会影响iNOS mRNA水平引起的IL-1β触发的增加。现在我们研究了地塞米松抑制系膜细胞中IL-1β刺激的iNOS表达的机制。

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