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.
Keywords: LINC00943; MPP+; Parkinson’s disease; RAB3IP; miR-15b-5p; neuronal damage.