• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>RSC Advances >LncRNA MALAT1 aggravates MPP-induced neuronal injury by regulating miR-212 in SH-SY5Y cells
【24h】

LncRNA MALAT1 aggravates MPP-induced neuronal injury by regulating miR-212 in SH-SY5Y cells

机译：LncRNA MALAT1通过调节SH-SY5Y细胞中的miR-212加重MPP诱导的神经元损伤

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Parkinson's disease (PD) is the most common neurodegenerative disease and its incidence is rising. Long noncoding RNAs (lncRNAs) have been reported to have essential roles in development of PD. LncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is dysregulated in PD, while the role of MALAT1 and its mechanism in PD remain poorly understood. In this study, SH-SY5Y cells were exposed to 1-methyl-4-phenylpyridinium (MPP ~(+) ) to induce a PD model in vitro . Then we explored the effect of MALAT1 on cell viability, apoptosis and inflammatory response as well as its interaction with miR-212 in MPP ~(+) -treated SH-SY5Y cells. The results showed that MALAT1 was up-regulated in MPP ~(+) -treated SH-SY5Y cells compared with that in the normal group. Overexpression of MALAT1 exacerbated MPP ~(+) -induced neuronal injury, uncovered by inhibition of cell viability and increase of cell apoptosis as well as inflammatory cytokine expressions in SH-SY5Y cells. However, knockdown of MALAT1 exerted the opposite effect in MPP ~(+) -treated SH-SY5Y cells. Moreover, MALAT1 was bound to miR-212 and negatively regulated the miR-212 level. Furthermore, addition of miR-212 ablated the regulatory effect of MALAT1 on MPP ~(+) -induced neuronal injury, as indicated by restoration of cell viability and lower apoptotic rate along with inflammatory cytokine levels in SH-SY5Y cells. Therefore, we concluded that MALAT1 exacerbated MPP ~(+) -induced neuronal injury through regulating cell viability, apoptosis and inflammatory cytokines by sponging miR-212, providing a novel theoretical foundation for application of MALAT1 in PD.
机译：帕金森氏病（PD）是最常见的神经退行性疾病，其发病率正在上升。据报道，长的非编码RNA（lncRNA）在PD的发展中具有重要作用。 LncRNA转移相关的肺腺癌转录本1（MALAT1）在PD中失调，而MALAT1的作用及其在PD中的机制仍知之甚少。在这项研究中，SH-SY5Y细胞暴露于1-甲基-4-苯基吡啶鎓（MPP〜（+））以在体外诱导PD模型。然后，我们探讨了MALAT1对MPP〜（+）处理的SH-SY5Y细胞中细胞活力，凋亡和炎症反应以及与miR-212相互作用的影响。结果显示，与正常组相比，在MPP〜（+）处理的SH-SY5Y细胞中MALAT1上调。 MALAT1的过表达加剧了MPP〜（+）诱导的神经元损伤，其通过抑制细胞活力和增加细胞凋亡以及SH-SY5Y细胞中炎性细胞因子的表达得以揭示。但是，敲低MALAT1在MPP〜（+）处理的SH-SY5Y细胞中发挥相反的作用。此外，MALAT1绑定到miR-212，并负调控miR-212的水平。此外，miR-212的添加消除了MALAT1对MPP〜（+）诱导的神经元损伤的调节作用，如SH-SY5Y细胞中细胞活力的恢复和较低的凋亡率以及炎性细胞因子水平所表明的。因此，我们得出的结论是，MALAT1通过刺激miR-212来调节细胞活力，凋亡和炎性细胞因子，从而加剧了MPP〜（+）诱导的神经元损伤，为MALAT1在PD中的应用提供了新的理论基础。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号