miR-30b 通过 SNCA 保护黑质纹状体多巴胺能神经元免受 MPP (+) 诱导的神经毒性。
miR-30b protects nigrostriatal dopaminergic neurons from MPP(+)-induced neurotoxicity via SNCA.
机构信息
Institute of Neurology, The Second Affiliated Hospital of Jiaxing University, Jiaxing, China.
出版信息
Brain Behav. 2020 Apr;10(4):e01567. doi: 10.1002/brb3.1567. Epub 2020 Mar 10.
OBJECTIVE
To explore the function of miR-30b in pathogenesis of Parkinson's disease (PD) and its underlying molecular mechanism.
MATERIALS AND METHODS
We used 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPP(+)) as a tool for constructing the PD cell model, using miR-30b mimics or inhibitors to manipulate miR-30b level for an experimental model of acquisition. The cell viability of SH-SY5Y was detected by CCK, and luciferase was used to screen the binding of target genes. The protein levels of SNCA were measured by Western blot. Then, we investigate the changes in pro- and anti-apoptotic markers with or without miR-30b treatment.
RESULTS
There was a significant low expression of MiR-30b in MPP(+)-induced cells. SH-SY5Y cell viability was rescued by MiR-30b overexpression. Luciferase experiments showed that MiR-30b may bind to the 3'-UTR side of SNCA and inhibited its expression. By Western blot, the SNCA level was markedly decreased by miR-30b. miR-30b attenuated the upregulation of Bax and the depletion of Bcl-2 induced by MPP(+).
目的
探讨 miR-30b 在帕金森病（PD）发病机制中的作用及其潜在的分子机制。
材料和方法
我们使用 1-甲基-4-苯基-1,2,3,6-四氢吡啶（MPP(+)) 作为构建 PD 细胞模型的工具，使用 miR-30b 模拟物或抑制剂来操纵 miR-30b 水平，以获得获得性实验模型。通过 CCK 检测 SH-SY5Y 的细胞活力，并使用荧光素酶筛选靶基因的结合。通过 Western blot 测量 SNCA 的蛋白水平。然后，我们研究了在有无 miR-30b 处理的情况下，促凋亡和抗凋亡标记物的变化。
结果
MPP(+)-诱导的细胞中 miR-30b 的表达明显降低。MiR-30b 的过表达挽救了 SH-SY5Y 细胞的活力。荧光素酶实验表明，MiR-30b 可能结合到 SNCA 的 3'-UTR 侧并抑制其表达。通过 Western blot，MiR-30b 显著降低了 SNCA 水平。MiR-30b 减弱了 MPP(+)诱导的 Bax 的上调和 Bcl-2 的耗竭。
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