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首页> 外文期刊>Cellular Physiology and Biochemistry >MiR-21 Regulates TNF-?±-Induced CD40 Expression via the SIRT1-NF-?oB Pathway in Renal Inner Medullary Collecting Duct Cells
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MiR-21 Regulates TNF-?±-Induced CD40 Expression via the SIRT1-NF-?oB Pathway in Renal Inner Medullary Collecting Duct Cells

机译：MiR-21通过SIRT1-NF-ΔoB途径调节肾内髓质收集导管细胞中TNF-α±诱导的CD40表达。

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>Background/Aims: Recent studies have indicated that microRNA-21 (miR-21) is involved in the inflammatory response in relation to renal disease. Sirtuin1 (SIRT1) exerts renoprotective properties by counteracting inflammation. The activation of CD40 triggers inflammation that participates in renal inflammation and injury. The relationship between miR-21, SIRT1 and CD40, however, remains elusive. Methods: Immunohistochemistry, small-interfering RNA (siRNA) transfection, quantitative real-time PCR and western blotting were applied to assess the morphological, functional and molecular mechanisms in primary cultured renal inner medullary collecting duct (IMCD) cells. Results: TNF-?± induced miR-21, CD40 and acetylated-NF-?oBp65 (Ac-p65) expressions and reduced SIRT1 expression in IMCD cells. miR-21 mimics increased SIRT1 expression and attenuated Ac-p65 and CD40 expressions in TNF-?±-induced IMCD cells, and the corresponding changes were observed with a miR-21 inhibitor. SIRT1 overexpression or activation by SRT1720 diminished TNF-?±-induced CD40 and Ac-p65 expressions, which was reversed by SIRT1 siRNA or the inhibitors Ex527 and sirtinol and augmented by pretreatment with NF-?oB siRNA. Further study found that the inhibitory effect of miR-21 on Ac-p65 and CD40 expressions was impeded by pretreatment with SIRT1 siRNA. Conclusion: The present study indicates that miR-21 inhibits TNF-?±-induced CD40 expression in IMCD cells via the SIRT1-NF-?oB signalling pathway, which provides new insight in understanding the anti-inflammatory effect of miR-21.
机译：> 背景/目标： 最近的研究表明，microRNA-21（miR-21）参与了与肾脏疾病相关的炎症反应。 Sirtuin1（SIRT1）通过抵抗炎症发挥肾脏保护作用。 CD40的激活触发炎症，该炎症参与肾脏炎症和损伤。但是，miR-21，SIRT1和CD40之间的关系仍然难以捉摸。 方法 ： 分别是免疫组织化学，小干扰RNA（siRNA）转染，定量实时PCR和蛋白质印迹用于评估原代培养的肾脏内髓收集管（IMCD）细胞的形态，功能和分子机制。 结果 TNF-α±诱导miR-21，CD40和乙酰化NF-αoBp65（Ac- p65）表达和IMCD细胞中SIRT1表达降低。 miR-21模拟物在TNF-α诱导的IMCD细胞中增加了SIRT1表达，并减弱了Ac-p65和CD40表达，并且用miR-21抑制剂观察到了相应的变化。 SIRT1的过表达或SRT1720的激活减少了TNF-α-诱导的CD40和Ac-p65的表达，这被SIRT1 siRNA或抑制剂Ex527和sirtinol逆转，并通过NF-κBsiRNA预处理而增强。进一步的研究发现，用SIRT1 siRNA预处理可抑制miR-21对Ac-p65和CD40表达的抑制作用。 结论 ：本研究表明miR-21通过SIRT1-NF-αoB信号通路抑制IMCD细胞中TNF-α±诱导的CD40表达，这提供了新的途径。了解miR-21的抗炎作用的见识。

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