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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Endonuclease Vlll-like 3 (Neil3) DNA glycosylase promotes neurogenesis induced by hypoxia-ischemia
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Endonuclease Vlll-like 3 (Neil3) DNA glycosylase promotes neurogenesis induced by hypoxia-ischemia

机译：核酸内切酶Vlll样3（Neil3）DNA糖基化酶促进缺氧缺血诱导的神经发生

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摘要

Neural stem/progenitor cell proliferation and differentiation are required to replace damaged neurons and regain brain function after hypoxic-ischemic events. DNA base lesions accumulating during hypoxic-ischemic stress are removed by DNA glycosylases in the base-excision repair pathway to prevent cytotoxicity and mutagen-esis. Expression of the DNA glycosylase endonuclease Vlll-like 3 (Neil3) is confined to regenerative subregions in the embryonic and perinatal brains. Here we show profound neuropathology in Neil3-knockout mice characterized by a reduced number of micro-glia and loss of proliferating neuronal progenitors in the striatum after hypoxia-ischemia. In vitro expansion of Neil3-deficient neural stem/progenitor cells revealed an inability to augment neurogenesis and a reduced capacity to repair for oxidative base lesions in single-stranded DNA. We propose that Neil3 exercises a highly specialized function through accurate molecular repair of DNA in rapidly proliferating cells.
机译：在缺氧缺血事件后，需要神经干/祖细胞增殖和分化来替换受损的神经元并恢复脑功能。在缺氧缺血性应激期间积累的DNA碱基损伤可通过碱基切除修复途径中的DNA糖基化酶去除，以防止细胞毒性和诱变。 DNA糖基化酶内切核酸酶VIII-3（Neil3）的表达仅限于胚胎和围生期大脑中的再生子区域。在这里，我们展示了Neil3基因敲除小鼠的深层神经病理学，其特征为缺氧缺血后纹状体中的小胶质细胞减少和增殖性神经元祖细胞的丢失。缺乏Neil3的神经干/祖细胞的体外扩增显示，无法增强神经发生，修复单链DNA中的氧化性碱基损伤的能力却下降。我们建议Neil3通过快速增殖细胞中的DNA的精确分子修复来行使高度专门化的功能。

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    Yngve Sejersted; Gunn A. Hildrestrand; David Kunke; Veslemoy Rolseth; Silje Z. Krokeide; Christine G. Neurauter; Rajikala Suganthan; Monica Atneosen-Asegg; Aaron M. Fleming; Ola D. Saugstad; Cynthia J. Burrows; Luisa Luna; Magnar BJoras;

  • 作者单位

    Departments of Microbiology University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Departments of Pediatric Research, University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Departments of Centre for Molecular Biology and Neuroscience,University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway;

    Departments of Microbiology University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Departments of Centre for Molecular Biology and Neuroscience,University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway;

    Departments of Microbiology University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Departments of Centre for Molecular Biology and Neuroscience,University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Institute for Surgical Research, Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway;

    Departments of Microbiology University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Departments of Centre for Molecular Biology and Neuroscience,University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway;

    Departments of Microbiology University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Departments of Centre for Molecular Biology and Neuroscience,University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway;

    Departments of Microbiology University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Departments of Centre for Molecular Biology and Neuroscience,University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway;

    Departments of Microbiology University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Departments of Centre for Molecular Biology and Neuroscience,University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway;

    Departments of Pediatric Research, University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway;

    Department of Chemistry, University of Utah, Salt Lake City, UT 84112;

    Departments of Pediatric Research, University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway;

    Department of Chemistry, University of Utah, Salt Lake City, UT 84112;

    Departments of Microbiology University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Departments of Centre for Molecular Biology and Neuroscience,University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway;

    Departments of Microbiology University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Departments of Centre for Molecular Biology and Neuroscience,University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway,Departments of Institute of Clinical Biochemistry, University of Oslo and Oslo University Hospital, Rikshospitalet, Nydalen, N-0424 Oslo, Norway;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    DNA damage; formamidopyrimidine-DNA glycosylase/endonudease VIII hydantoins; neural stem cells; neuronal progenitor cells;

    机译：DNA损伤;甲酰嘧啶-DNA糖基化酶/内切酶VIII乙内酰脲;神经干细胞神经元祖细胞;
  • 入库时间 2022-08-18 00:41:00

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