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首页> 外文期刊>Journal of Cellular Physiology >MicroRNA‐224‐5p regulates adipocyte apoptosis induced by TNFα via controlling NF‐κB activation
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MicroRNA‐224‐5p regulates adipocyte apoptosis induced by TNFα via controlling NF‐κB activation

机译：微rna量224 5 p调节脂肪细胞的凋亡诱导,通过控制NF肿瘤坏死因子ακB激活

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摘要

Tumor necrosis factor (TNF) α can induce cell apoptosis and activate nuclear transcription (NF)‐κB in different cell types. Activated NF‐κB further promotes or suppresses cellular apoptosis in different cases. The present study explored the effect of activated NF‐κB on adipocyte apoptosis induced by TNFα and which microRNAs (miRNAs) were involved in the process. Our findings demonstrated that treatment of differentiated 3T3‐L1 adipocytes with TNFα (20?ng/mL) rapidly activated NF‐κB and induced moderate apoptosis. Pyrrolidinedithiocarbamic acid (PDTC, 60?μM), a specific NF‐κB inhibitor, abated NF‐κB activation that rendered the adipocytes vulnerable to TNFα‐induced apoptosis. Dozens of miRNAs exhibited significant expression changes following TNFα treatment and the addition of PDTC. In which, miRNA‐224‐5p (miR‐224) was up‐regulated by TNFα exposure but down‐regulated by PDTC addition. Furthermore, over‐expression of miR‐224 promoted NF‐κB activation and prevented the adipocyte apoptosis induced by TNFα, while miR‐224 deficiency showed the opposite effects. The TRAF‐associated NF‐κB activator ( TANK ) gene was identified as a direct target of miR‐224 by computational and luciferase reporter assays. Additionally, silencing the TANK gene by the small interfering RNA similarly promoted NF‐κB activation and attenuated the cellular apoptosis. In conclusion, these findings demonstrate that miR‐224 plays an essential role in adipocyte apoptosis caused by TNFα through control of NF‐κB activation via targeting the TANK gene.
机译：肿瘤坏死因子(TNF)α可以诱导细胞细胞凋亡和激活核转录(NF)必经κB在不同的细胞类型。进一步促进或抑制细胞凋亡在不同的情况下。NFκB,其脂肪细胞激活的影响肿瘤坏死因子α诱导细胞凋亡和小分子核糖核酸(microrna)参与了这一过程。结果表明,治疗分化3 t3 L1脂肪细胞与肿瘤坏死因子α(20 ? ng / mL)迅速激活NFκB和诱导温和的细胞凋亡。酸(PDTC 60 ?μM),一个特定的NFκB抑制剂,减弱NFκB激活,呈现脂肪细胞容易受到肿瘤坏死因子α诱导细胞凋亡。许多microrna方面表现出显著的表达式随着肿瘤坏死因子α治疗和变化PDTC。量受肿瘤坏死因子α暴露但应承担监管PDTC加法。miR量224提升NFκB激活和预防脂肪细胞的肿瘤坏死因子α诱导细胞凋亡,而miR量224缺陷显示相反的效果。TRAF检测相关地理NFκB催化剂(坦克)基因被认定为直接目标的米尔还是224年计算和荧光素酶记者化验。此外,坦克基因沉默的小干扰RNA同样促进了NFκB激活和减毒细胞凋亡。总之,这些发现证明米尔224在脂肪细胞中起着至关重要的作用通过控制细胞凋亡引起的肿瘤坏死因子αNFκB通过针对坦克基因激活。

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