当前位置: X-MOL 学术Neurol. Res. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
LINC00943 knockdown attenuates MPP+-induced neuronal damage via miR-15b-5p/RAB3IP axis in SK-N-SH cells
Neurological Research ( IF 1.9 ) Pub Date : 2020-11-19 , DOI: 10.1080/01616412.2020.1834290
Chunming Meng 1 , Jing Gao 1 , Qingyuan Ma 1 , Qian Sun 1 , Tiantian Qiao 1
Affiliation  

ABSTRACT

Objectives

Parkinson’s disease (PD) is a neurodegenerative problem correlated with neuronal damage. Long noncoding RNAs (lncRNAs) are implicated in neuronal damage in PD development. This research aims to analyze the function and mechanism of LINC00943 in 1-methyl-4-phenylpyridinium (MPP+)-caused neuronal injury.

Methods

MPP+-challenged SK-N-SH cells served as a PD-like model of neuronal damage. LINC00943, microRNA-15b-5p (miR-15b-5p) and RAB3A interacting protein (RAB3IP) abundances were examined via quantitative reverse transcription polymerase chain reaction or western blot. MPP+-caused neuronal damage was assessed via cell viability, apoptosis, inflammatory injury and oxidative injury. The association between miR-15b-5p and LINC00943 or RAB3IP was determined via dual-luciferase reporter analysis and RNA immunoprecipitation.

Results

LINC00943 abundance was up-regulated in MPP+-challenged SK-N-SH cells. LINC00943 silence alleviated MPP+-caused decrease of cell viability and elevation of apoptosis, inflammatory injury and oxidative injury. miR-15b-5p was inhibited via LINC00943, and miR-15b-5p inhibition reversed knockdown of LINC00943-mediated suppression of MPP+-induced neuronal damage. RAB3IP was targeted via miR-15b-5p, and LINC00943 could regulate RAB3IP via miR-15b-5p. miR-15b-5p addition mitigated MPP+-induced neuronal damage through decreasing RAB3IP.

Conclusion

LINC00943 inhibition alleviated MPP+-induced neuronal injury via miR-15b-5p/RAB3IP axis, indicating a potential target for treatment of PD.



中文翻译:

LINC00943 敲低通过 SK-N-SH 细胞中的 miR-15b-5p/RAB3IP 轴减轻 MPP+ 诱导的神经元损伤

摘要

目标

帕金森病 (PD) 是一种与神经元损伤相关的神经退行性疾病。长链非编码 RNA (lncRNA) 与 PD 发展中的神经元损伤有关。本研究旨在分析LINC00943在1-甲基-4-苯基吡啶鎓(MPP +)引起的神经元损伤中的作用和机制。

方法

MPP +攻击的 SK-N-SH 细胞充当神经元损伤的 PD 样模型。通过定量逆转录聚合酶链反应或蛋白质印迹检查 LINC00943、microRNA-15b-5p(miR-15b-5p)和 RAB3A 相互作用蛋白(RAB3IP)丰度。MPP + 引起的神经元损伤通过细胞活力、细胞凋亡、炎症损伤和氧化损伤进行评估。miR-15b-5p 与 LINC00943 或 RAB3IP 之间的关联是通过双荧光素酶报告基因分析和 RNA 免疫沉淀确定的。

结果

LINC00943 丰度在 MPP +攻击的 SK-N-SH 细胞中上调。LINC00943沉默减轻了MPP + -引起的细胞活力降低和细胞凋亡、炎症损伤和氧化损伤的升高。miR-15b-5p 被 LINC00943 抑制,并且 miR-15b-5p 抑制逆转了 LINC00943 介导的 MPP +诱导的神经元损伤抑制的敲低。RAB3IP 通过 miR-15b-5p 靶向,LINC00943 可以通过 miR-15b-5p 调节 RAB3IP。添加 miR-15b-5p通过降低 RAB3IP减轻 MPP +诱导的神经元损伤。

结论

LINC00943 抑制通过 miR-15b-5p/RAB3IP 轴减轻 MPP +诱导的神经元损伤,表明治疗 PD 的潜在靶点。

更新日期:2020-11-19
down
wechat
bug