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首页> 外文期刊>RSC Advances >MiR-19b alleviates MPP+-induced neuronal cytotoxicity via targeting the HAPLN4/MAPK pathway in SH-SY5Y cells
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MiR-19b alleviates MPP+-induced neuronal cytotoxicity via targeting the HAPLN4/MAPK pathway in SH-SY5Y cells

机译：MiR-19B通过靶向SH-SY5Y细胞中的HAPLN4 / MAPK途径来减轻MPP +-诱导的神经元细胞毒性

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Background: miR-19b has been reported to be involved in nervous system disease including Parkinson's disease (PD). However its molecular basis has not been exhaustively elucidated. Materials and Methods: SH-SY5Y cells were treated with 1-methyl-4-phenylpyridinium (MPP+) to construct PD model in vitro. RT-qPCR was performed to detect the expression of miR-19b and proteoglycan link protein 4 (HAPLN4) mRNA. Western blot analysis was used to measure the level of HAPLN4 and mitogen activated protein kinase (MAPK)-related protein. Cell viability and apoptosis were determined by MTT and flow cytometry. Commercial ELISA kits were applied to quantify caspase-3 activity, lactate dehydrogenase (LDH), reactive oxygen species (ROS), superoxide dismutase (SOD), tumor necrosis factor- (TNF-) and interleukin-1 beta (IL-1). Dual-luciferase reporter assay was applied to assess the relationship between miR-19b and HAPLN4. Results: miR-19b was downregulated in MPP+-induced SH-SY5Y cells. miR-19b overexpression reversed MPP+-induced suppression of cell viability and promotion of cell apoptosis in SH-SY5Y cells. Moreover, miR-19b alleviated MPP+-induced cytotoxicity of SH-SY5Y cells, embodied by the decrease of LDH release, caspase-3 activity, ROS expression, TNF- and IL-1 secretion, as well as the increase of SOD level. HAPLN4 was identified as a direct target of miR-19b and miR-19b repressed HAPLN4 expression in a post-transcriptional manner. In addition, miR-19b-mediated anti-apoptosis effect was abated following HAPLN4 expression restoration in MPP+-induced SH-SY5Y cells. Furthermore, MAPK signaling participated in miR-19b/HAPLN4-mediated regulation in MPP+-treated SH-SY5Y cells. Conclusion: the neuroprotective effect of miR-19b might be mediated by HAPLN4/MAPK pathway in SH-SY5Y cells.
机译：背景：据报道MiR-19B涉及神经系统疾病，包括帕金森病（PD）。然而，它的分子基础并未被详尽阐释。材料和方法：用1-甲基-4-苯基吡啶（MPP +）处理SH-SY5Y细胞以在体外构建PD模型。进行RT-QPCR以检测miR-19b和蛋白多糖链路蛋白4（hapln4）mRNA的表达。用于测量HAPLN4和丝裂原活化蛋白激酶（MAPK）相关蛋白水平的蛋白质印迹分析。通过MTT和流式细胞术测定细胞活力和细胞凋亡。应用商业ELISA试剂盒来量化Caspase-3活性，乳酸脱氢酶（LDH），反应性氧物质（ROS），超氧化物歧化酶（SOD），肿瘤坏死因子（TNF-）和白细胞介素-1β（IL-1）。施用双荧光素酶报告器测定以评估miR-19b和hapln4之间的关系。结果：MIR-19B在MPP +-诱导的SH-SY5Y细胞中下调。 miR-19b过表达逆转MPP +诱导细胞活力和促进SH-SY5Y细胞细胞凋亡的抑制。此外，MIR-19B缓解了MPP +-诱导了SH-SY5Y细胞的细胞毒性，其通过LDH释放，Caspase-3活性，ROS表达，TNF和IL-1分泌的降低而体现，以及SOD水平的增加。 HAPLN4被鉴定为miR-19b和miR-19b的直接靶标以转录后的方式以术后的方式抑制HAPLN4表达。此外，在MPP +-诱导的SH-SY5Y细胞中，在HAPLN4表达恢复之后减少miR-19B介导的抗凋亡效应。此外，MAPK信号传导参与MIR-19B / HAPLN4介导的MPP +-治疗SH-SY5Y细胞调节。结论：MIR-19B的神经保护作用可能是SH-SY5Y细胞中HAPLN4 / MAPK途径介导的。

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  • 来源
    《RSC Advances》 |2018年第19期|共9页
  • 作者

    Liu Wei; Geng Lijiao; Chen Yong;

  • 作者单位

    Henan Univ Dept Neurol Huaihe Hosp Kaifeng 475000 Peoples R China;

    Henan Univ Dept Neurol Huaihe Hosp Kaifeng 475000 Peoples R China;

    Henan Univ Dept Rehabil Med Huaihe Hosp 357 Ximen St Kaifeng 475000 Peoples R China;

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  • 正文语种 eng
  • 中图分类 化学;
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