Background
Parkinson's disease (PD) is a common neurodegenerative movement disorder, but the pathogenesis is still unclear. Long non-coding RNAs (lncRNAs) have been reported to play a prominent role in PD.
Conclusions
LINC00943 knockdown could attenuate MPP+-triggered neuron injury by regulating the miR-7-5p/CXCL12 axis, hinting at a promising therapeutic target for PD treatment.
Methods
LINC00943, microRNA-7-5p (miR-7-5p), and the chemokine (C-X-C motif) ligand 12 (CXCL12, also referred to as SDF-1) level were examined by real-time quantitative polymerase chain reaction (RT-qPCR). Cell viability and apoptosis were analyzed by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT), and flow cytometry assays, severally. Protein levels of interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and CXCL12 were assessed by western blot assay. The ROS generation and SOD activity were detected by the corresponding kits. The binding relationship between miR-7-5p and LINC00943 or CXCL12 was predicted by Starbase and then verified by a dual-luciferase reporter and RNA Immunoprecipitation (RIP) assays.
Objective
This study is designed to explore the role and mechanism of long intergenic non-coding RNA 00943 (LINC00943) in the N-methyl-4-phenylpyridine (MPP+)-inducted PD model.
Results
LINC00943 and CXCL12 were increased, and miR-7-5p was decreased in MPP+-inducted SK-N-SH cells. LINC00943 silencing promoted cell viability, and repressed apoptosis and the inflammatory response in MPP+-treated SK-N-SH cells. The mechanical analysis discovered that LINC00943 acted as a sponge of miR-7-5p to regulate CXCL12 expression. Conclusions: LINC00943 knockdown could attenuate MPP+-triggered neuron injury by regulating the miR-7-5p/CXCL12 axis, hinting at a promising therapeutic target for PD treatment.