Research Article

检查miR-23a在耐热性发展中的作用

卷 20, 期 3, 2020

页: [194 - 201] 页: 8

弟呕挨: 10.2174/1566524019666191021111028

价格: $65

摘要

背景:耐热性是在暴露于非致命蛋白毒性应力后发生的,耐热性增强的一种获得状态。大量证据表明,属于热休克蛋白家族的分子伴侣分子可能是耐热状态的潜在介体。 目的:最近的证据表明,热休克蛋白HSP90,HSP70和HSP27通过在应激诱导的凋亡途径中的各个步骤进行干预,抑制了热诱导的细胞死亡。先前的研究表明,HSP70通过阻止MCL-1水平的NOXA依赖性下降(导致BAX激活和线粒体细胞色素c释放)来防止热诱导的细胞凋亡。我们还证明了表达HSP70的细胞具有增强的miR-23a水平,可以防止热诱导的NOXA水平增加并抑制细胞凋亡。 方法:使用RT-PCR和半定量RT-PCR对稳定表达对照shRNA或靶向miRNA的miR-23a稳定转染的细胞系进行定量,以确定不同的高温暴露处理对miR-23a和Noxa mRNA表达水平的影响。 结果:这项研究表明耐热诱导的预热休克治疗能够增加miR-23a的水平。此外,表达具有降低的miR-23a水平的表达靶向miR-23a的shRNA的稳定细胞克隆不能形成耐热状态,从而导致细胞凋亡。 结论:这些结果证明了miR-23a是耐热状态发展的重要因素这一新颖发现。

关键词: 耐热性,细胞凋亡,热休克蛋白,热疗,HSP70,NOXA,miR-23ª。

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