首页> 外文期刊>DNA and Cell Biology >microRNA-7 Protects Against 1-Methyl-4-Phenylpyridinium Iodide-Induced Cell Apoptosis in SH-SY5Y Cells by Directly Targeting Krupple-Like Factor 4
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microRNA-7 Protects Against 1-Methyl-4-Phenylpyridinium Iodide-Induced Cell Apoptosis in SH-SY5Y Cells by Directly Targeting Krupple-Like Factor 4

机译:microRNA-7通过直接靶向Krupple-like因子4来保护SH-SY5Y细胞中1-甲基-4-苯基吡啶鎓碘化物诱导的细胞凋亡

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摘要

This study intended to investigate the role and underling mechanism of microRNA-7 (miR-7) on neuronal death in Parkinson's disease (PD). Human neuroblastoma cell line SH-SY5Y was employed and 1-methyl-4-phenylpyridinium iodide [MPP(+)] was used to generate PD model in vitro. Furthermore, an upregulation of miR-7 was performed in SH-SY5Y by transfection with miR-7 mimics. Cell viability and cell apoptosis were determined. Moreover, the target and the mechanism of miR-7 in MPP(+)-induced cell death were also investigated. The upregulation of miR-7 promoted cell viability and suppressed cell apoptosis in MPP(+)-treated SH-SY5Y cells. Furthermore, miR-7 could directly bind to the 3-untranslated region of Kruppel-like factor 4 (KLF4, positions 574-580). Moreover, knockdown of KLF4 by the specific siRNA inhibited SH-SY5Y apoptosis under MPP(+) treatment. In addition, KLF4 overexpression apparently attenuated the protective effect of miR-7 in MPP(+)-induced SH-SY5Y apoptosis. This study indicated that miR-7 protects from MPP(+)-induced cell apoptosis in SH-SY5Y by directly targeting KLF4.
机译:这项研究旨在调查微RNA-7(miR-7)在帕金森氏病(PD)神经元死亡中的作用和潜在机制。使用人神经母细胞瘤细胞系SH-SY5Y,并使用1-甲基-4-苯基碘化碘[MPP(+)]体外生成PD模型。此外,通过用miR-7模拟物转染在SH-SY5Y中进行了miR-7的上调。测定细胞活力和细胞凋亡。此外,还研究了miR-7在MPP(+)诱导的细胞死亡中的靶标和机制。在MPP(+)处理的SH-SY5Y细胞中,miR-7的上调促进了细胞活力并抑制了细胞凋亡。此外,miR-7可以直接结合Kruppel样因子4的3个非翻译区(KLF4,位置574-580)。此外,在MPP(+)处理下,通过特异性siRNA敲低KLF4可以抑制SH-SY5Y细胞凋亡。此外,KLF4过表达显然减弱了miR-7在MPP(+)诱导的SH-SY5Y细胞凋亡中的保护作用。这项研究表明,miR-7通过直接靶向KLF4来保护免受MPP(+)诱导的SH-SY5Y细胞凋亡。

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