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Protective mechanisms of microRNA-27a against oxygen-glucose deprivation-induced injuries in hippocampal neurons

机译:microRNA-27a对氧葡萄糖剥夺所致海马神经元损伤的保护机制

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摘要

Hypoxic injuries during fetal distress have been shown to cause reduced expression of microRNA-27a (miR-27a), which regulates sensi-tivity of cortical neurons to apoptosis. We hypothesized that miR-27a overexpression attenuates hypoxia-and ischemia-induced neuronal apoptosis by regulating FOXO1, an important transcription factor for regulating the oxidative stress response. miR-27a mimic was transfected into hippocampal neurons to overexpress miR-27a. Results showed increased hippocampal neuronal viability and decreased caspase-3 ex-pression. The luciferase reporter gene system demonstrated that miR-27a directly binded to FOXO1 3′UTR in hippocampal neurons and inhibited FOXO1 expression, suggesting that FOXO1 was the target gene for miR-27a. These ifndings conifrm that miR-27a protects hippo-campal neurons against oxygen-glucose deprivation-induced injuries. The mechanism might be mediated by modulation of FOXO1 and apoptosis-related gene caspase-3 expression.
机译:已经显示出胎儿窘迫期间的缺氧损伤导致MicroRNA-27a(miR-27a)的表达减少,这调节皮质神经元对细胞凋亡的感觉。我们假设miR-27a过表达通过调节FoxO1来衰减缺氧和缺血诱导的神经元细胞凋亡,这是调节氧化应激反应的重要转录因子。 MiR-27A模拟被转染到海马神经元中以过表达miR-27a。结果表明,海马神经元活力增加,降低了Caspase-3前压力。荧光素酶报告基因系统证明miR-27a在海马神经元中直接结合FoxO1 3'UTR并抑制FoxO1表达,表明FoxO1是miR-27a的靶基因。这些IFNDINGS COIFRM认为miR-27a保护河马神经元免受氧葡萄糖剥夺诱导的伤害。该机制可能通过FOXO1和凋亡相关基因Caspase-3表达的调节来介导。

著录项

  • 来源
    《中国神经再生研究(英文版)》 |2016年第8期|1285-1292|共8页
  • 作者单位

    Department of Neonatology, Children’s Hospital of Soochow University, Suzhou, Jiangsu Province, China;

    Department of Emergency, Afifliated Hospital of Nantong University, Nantong, Jiangsu Province, China;

    Medical College of Nantong University, Nantong, Jiangsu Province, China;

    Department of Neonatology, Children’s Hospital of Soochow University, Suzhou, Jiangsu Province, China;

  • 收录信息 中国科学引文数据库(CSCD);中国科技论文与引文数据库(CSTPCD);
  • 原文格式 PDF
  • 正文语种 eng
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