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首页> 外文期刊>DNA and Cell Biology >-8-Oxoguanine DNA Glycosylase Overexpression Reduces Oxidative Stress-Induced Mitochondrial Dysfunction and Apoptosis Through the JNK Signaling Pathway in Human Bronchial Epithelial Cells
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-8-Oxoguanine DNA Glycosylase Overexpression Reduces Oxidative Stress-Induced Mitochondrial Dysfunction and Apoptosis Through the JNK Signaling Pathway in Human Bronchial Epithelial Cells

机译:-8-氧通DNA糖基酶过表达减少了通过人支气管上皮细胞的JNK信号通路通过JNK信号通路减少了氧化应激诱导的线粒体功能障碍和凋亡

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摘要

8-Oxoguanine DNA glycosylase (OGG1) is responsible for repairing 8-oxo-7,8-dihydroguanine (8-oxoG). Our previous study demonstrated that -OGG1 protects cells from oxidative damage-induced apoptosis and mitochondrial dysfunction in human lung cancer cells. However, the function of -OGG1 remains to be elucidated. In this study, we demonstrated that overexpressed -OGG1 has the same role as -OGG1 in protecting human bronchial epithelial cells from apoptosis and mitochondrial dysfunction. Furthermore, flow cytometry, confocal microscopy, and western blotting showed that the overexpression of -OGG1 could block oxidant-induced apoptosis in human bronchial epithelial cells. Additionally, knocking down OGG1 enhanced oxidative damage-induced apoptosis and mitochondrial dysfunction, whereas the overexpression of -OGG1 had the opposite effects and led to the downregulation of Bax and PARP. The antiapoptotic function of -OGG1 involved the JNK signaling pathway. These findings suggest that -OGG1 and -OGG1 have a similar function on preventing oxidative damage-mediated apoptosis and mitochondrial dysfunction; these effects might be important in the molecular events underlying oxidant-induced cytotoxicity.
机译:8-氧基川DNA糖基糖酶(OGG1)负责修复8-氧代-7,8-二氢胍(8- oxog)。我们以前的研究表明,-ogg1保护来自人肺癌细胞中氧化损伤诱导的细胞凋亡和线粒体功能障碍的细胞。但是,-ogg1的功能仍有待阐明。在这项研究中,我们证明过表达-OgG1在保护人支气管上皮细胞免受细胞凋亡和线粒体功能障碍中具有与-ogg1相同的作用。此外,流式细胞术,共聚合显微镜和蛋白质印迹表明,-ogg1的过表达可以阻断人支气管上皮细胞中的氧化剂诱导的细胞凋亡。此外,敲击OGG1增强的氧化损伤诱导的细胞凋亡和线粒体功能障碍,而-ogg1的过表达具有相反的效果并导致BAX和PARP的下调。 -ogg1的抗曝光功能涉及JNK信号通路。这些研究结果表明 - 古代和-ogg1在预防氧化损伤介导的细胞凋亡和线粒体功能障碍方面具有类似的功能。这些效果在氧化剂诱导的细胞毒性下面的分子事件中可能是重要的。

著录项

  • 来源
    《DNA and Cell Biology》 |2017年第12期|共10页
  • 作者单位

    Guangdong Med Univ Affiliated Hosp Clin Res Ctr Zhanjiang 524001 Peoples R China;

    Guangdong Med Univ Affiliated Hosp Clin Res Ctr Zhanjiang 524001 Peoples R China;

    Guangdong Med Univ Affiliated Hosp Clin Res Ctr Zhanjiang 524001 Peoples R China;

    Guangdong Med Univ Affiliated Hosp Clin Res Ctr Zhanjiang 524001 Peoples R China;

    Guangdong Med Univ Affiliated Hosp Clin Res Ctr Zhanjiang 524001 Peoples R China;

    Guangdong Med Univ Affiliated Hosp Clin Res Ctr Zhanjiang 524001 Peoples R China;

    Guangdong Med Univ Affiliated Hosp Clin Res Ctr Zhanjiang 524001 Peoples R China;

    Guangdong Med Univ Affiliated Hosp Dept Resp Med Zhanjiang Peoples R China;

    Guangdong Med Univ Affiliated Hosp Dept Resp Med Zhanjiang Peoples R China;

    Guangdong Med Univ Affiliated Hosp Clin Res Ctr Zhanjiang 524001 Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞遗传学;
  • 关键词

    -OGG1; mitochondrial dysfunction; apoptosis; JNK signaling pathway; BEAS-2B;

    机译:-ogg1;线粒体功能障碍;细胞凋亡;JNK信号通路;BEAS-2B;

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