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首页> 外文期刊>Cell cycle >LncRNA MIAT overexpression reduced neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury through miR-211/GDNF
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LncRNA MIAT overexpression reduced neuron apoptosis in a neonatal rat model of hypoxic-ischemic injury through miR-211/GDNF

机译:LNCRNA MIAT过度表达通过MIR-211 / GDNF降氧缺氧损伤的新生大鼠模型中的神经元细胞凋亡降低

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摘要

Objective: To investigate the underlying mechanism of lncRNA myocardial infarction-associated transcript (MIAT) in hypoxic-ischemic (HI)-induced neonatal cerebral palsy. Materials and methods: Neonatal rat model of HI injury was established to detect the motor function. LncRNA MIAT, miR-211, glial cell line-derived neurotrophic factor (GDNF) and caspase-3 expressions were measured by qRT-PCR or western blot. The apoptosis of Neuro2A cells was detected by flow cytometry. RNA immunoprecipitation (RIP) and RNA pull-down assays were performed to confirm the interaction between MIAT and miR-211. Results: Compared with control group, lncRNA MIAT and GDNF were downregulated in striatal tissues of neonatal rats in HI group and oxygen glucose deprivation (OGD)-induced ischemic injury of Neuro2A cells, whereas miR-211 was up-regulated in striatal tissues of HI group and OGD-induced ischemic injury of Neuro2A cells. LncRNA MIAT interacted with miR-211, and lncRNA MIAT overexpression reduced neuron apoptosis through miR-211. Besides, GDNF expression was positively regulated by lncRNA MIAT and negatively regulated by miR-211 in Neuro2A cells. In vivo experiment proved MIAT promoted motor function and relieved HI injury. Conclusion: MIAT overexpression reduced apoptosis of Neuro2A cells through miR-211/GDNF, which relieved HI injury of neonatal rats.
机译:目的:探讨缺氧缺血(HI)诱导的新生儿脑瘫的LNCRNA心肌梗死相关转录(MIAI AIA)的潜在机制。材料和方法:建立了HI损伤的新生大鼠模型,以检测电动机功能。通过QRT-PCR或Western印迹测量LNCRNA MIAT,MIR-211,胶质细胞系衍生的神经营养因子(GDNF)和Caspase-3表达。通过流式细胞术检测神经2A细胞的凋亡。进行RNA免疫沉淀(RIP)和RNA下拉测定以确认MIAI和MIR-211之间的相互作用。结果:与对照组相比,LNCRNA MIAIA和GDNF在HI组和氧葡萄糖剥夺(OGD)的新生大鼠的纹状体组织中下调,诱导神经2A细胞的缺血性损伤,而MIR-211在HI的纹状体组织中上调群和OGD诱导的神经2A细胞缺血性损伤。 LNCRNA MIAT与miR-211相互作用,并且LNCRNA MIAI AIAI AIAT过表达通过MIR-211减少神经元细胞凋亡。此外,GDNF表达由LNCRNA Miat呈正调节,并通过神经2A细胞中的miR-211负调节。在体内实验中证明了MIAT促进了电机功能并缓解了HI损伤。结论:MIR-211 / GDNF的寿命过度表达降低了神经2A细胞的凋亡,其解毒了新生大鼠的Hi损伤。

著录项

  • 来源
    《Cell cycle》 |2019年第2期|共11页
  • 作者单位

    Zhengzhou Univ Affiliated Hosp 5 Key Lab Rehabil Med Henan Dept Children Rehabil Zhengzhou;

    Zhengzhou Univ Affiliated Hosp 5 Key Lab Rehabil Med Henan Dept Children Rehabil Zhengzhou;

    Zhengzhou Univ Affiliated Hosp 5 Key Lab Rehabil Med Henan Dept Children Rehabil Zhengzhou;

    Zhengzhou Univ Affiliated Hosp 5 Key Lab Rehabil Med Henan Dept Children Rehabil Zhengzhou;

    Zhengzhou Univ Affiliated Hosp 5 Key Lab Rehabil Med Henan Dept Children Rehabil Zhengzhou;

    Zhengzhou Univ Affiliated Hosp 5 Key Lab Rehabil Med Henan Dept Children Rehabil Zhengzhou;

    Zhengzhou Univ Affiliated Hosp 5 Key Lab Rehabil Med Henan Dept Children Rehabil Zhengzhou;

    Henan Prov Hosp TCM Cent Lab Zhengzhou Henan Peoples R China;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 细胞生物学;
  • 关键词

    MIAT; miR-211; GDNF; neonatal rat; hypoxic-ischemic injury; cerebral palsy;

    机译:miat;mir-211;gdnf;新生大鼠;缺氧缺血性损伤;脑瘫;

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