Geng Lijiao, Liu Wei, Chen Yong
1 Department of Rehabilitation Medicine, Huaihe Hospital of Henan University, Kaifeng 475000, China.
2 Department of Neurology, Huaihe Hospital of Henan University, Kaifeng 475000, China.
Exp Biol Med (Maywood). 2017 Dec;242(18):1757-1764. doi: 10.1177/1535370217734492. Epub 2017 Sep 29.
Ample evidence has demonstrated the involvement of microRNAs in Parkinson's disease pathogenesis. miR-124-3p was reported to be able to improve neural functional recovery. However, the underlying mechanism of miR-124-3p in Parkinson's disease progression was not well established. This study was designed to investigate the role of miR-124-3p in methyl phenyl pyridinium iodide (MPP)-induced SH-SY5Y cells, an in vitro Parkinson's disease model. It is observed that miR-124-3p expression was decreased, and STAT3 expression was increased in MPP-induced SH-SY5Y cells. miR-124-3p overexpression attenuated MPP-induced neuronal injury, displayed as increased cell viability and superoxide dismutase activities, as well as reduced cell apoptosis, Caspase-3 activity, lactate dehydrogenase activity, inflammatory factors TNF-α, and IL-1β levels and reactive oxygen species generation. Moreover, STAT3 was confirmed to be a miR-124-3p target. Restored STAT3 expression reversed miR-124-3p-induced neuroprotective effects against MPP-mediated neuronal injury. These data demonstrated that miR-124-3p contributed to neuroprotective effects in MPP-induced Parkinson's disease cell model by targeting STAT3. Impact statement PD affects millions of people in the world, causing uncontrolled tremors. MicroRNAs, a class of endogenous single-stranded non-coding transcript with approximately 22 nucleotides, could bind to the 3″ UTR of their targets. The functional action of miR-124-3p in PD was not fully elucidated. Our study found that ectopic expression miR-124-3p attenuated MPP-induced injury in PD model in vitro by suppressing neurotoxicity, neuronal apoptosis, neuroinflammation, and oxidative stress. Moreover, we validated that miR-124-3p could bind to STAT3 mediating the neuroprotective effect of miR-124-3p. We believe this study will be interesting for readers of this area.
大量证据表明，微小RNA参与了帕金森病的发病机制。据报道，miR-124-3p能够促进神经功能恢复。然而，miR-124-3p在帕金森病进展中的潜在机制尚未完全明确。本研究旨在探讨miR-124-3p在甲基苯基碘化吡啶（MPP）诱导的SH-SY5Y细胞（一种体外帕金森病模型）中的作用。研究发现，在MPP诱导的SH-SY5Y细胞中，miR-124-3p表达降低，而STAT3表达增加。miR-124-3p过表达减轻了MPP诱导的神经元损伤，表现为细胞活力和超氧化物歧化酶活性增加，细胞凋亡、Caspase-3活性、乳酸脱氢酶活性、炎症因子TNF-α和IL-1β水平以及活性氧生成减少。此外，证实STAT3是miR-124-3p的靶标。恢复STAT3表达可逆转miR-124-3p对MPP介导的神经元损伤的神经保护作用。这些数据表明，miR-124-3p通过靶向STAT3在MPP诱导的帕金森病细胞模型中发挥神经保护作用。影响声明 帕金森病影响着全球数百万人，导致无法控制的震颤。微小RNA是一类内源性单链非编码转录本，约有22个核苷酸，可与靶标的3″UTR结合。miR-124-3p在帕金森病中的功能作用尚未完全阐明。我们的研究发现，异位表达miR-124-3p通过抑制神经毒性、神经元凋亡、神经炎症和氧化应激，减轻了体外帕金森病模型中MPP诱导的损伤。此外，我们验证了miR-124-3p可与STAT3结合，介导miR-124-3p的神经保护作用。我们相信这项研究将引起该领域读者的兴趣。
