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Updated: Aug 10, 2026
A Simple Alternative to Stereotactic Injection for Brain Specific Knockdown of miRNA
Published on: December 26, 2015
LINC00943 knockdown attenuates MPP+-induced neuronal damage via miR-15b-5p/RAB3IP axis in SK-N-SH cells
Chunming Meng1, Jing Gao1, Qingyuan Ma1
1Department of Geriatrics, The First People's Hospital of Lianyungang , Lianyungan City, Jiangsu Province, China.
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.
