LncRNA SOX2-OT Participates in Parkinson’s Disease Through Regulating miRNA-942-5p/NAIF1 Axis
Abstract Parkinson’s disease (PD) is a neurodegenerative disease. Studies have shown that lncRNA SOX2-OT was highly expressed in PD patients, but its specific functions and mechanisms still need further research. This study aimed to explore whether lncRNA SOX2-OT could regulate oxidative stress, inflammation and neuronal apoptosis in PD in vitro model and explored the underlying mechanism. An in vitro PD cell model was induced by 1-methyl-4-phenylpyridinium (MPP+). The results of the biological software analysis and luciferase reporter assay indicated that miR-942-5p was a direct target of lncRNA SOX2-OT, and NAIF1 was a direct target of miR-942-5p. Experiments showed that the expression levels of lncRNA SOX2-OT and NAIF1 were increased, and miR-942-5p expression was decreased in SH-SY5Y cells following MPP+ treatment. In addition, MPP+ treatment reduced SH-SY5Y cell viability, induced apoptosis, increased cleaved-Caspase3 protein expression, and increased cleaved-Caspase3/Caspase3 ratio, increased LDH viability, and increased the levels of TNF-α, IL-1β and ROS in SH-SY5Y cells, reduced SOD activity, however, all these effects were inhibited by SOX2-OT-siRNA, and these inhibitions were reversed by miR-942-5p inhibitor. Moreover, the protective role of miR-942-5p mimic in MPP+ induced SH-SY5Y cells was significantly eliminated by NAIF1-plasmid. In summary, this study confirmed that lncRNA SOX2-OT regulated oxidative stress, inflammation and neuronal apoptosis via directly regulating the miR-942-5p/NAIF1 signal axis, and then participated in the occurrence and development of PD. These data provide a new potential targets for PD diagnosis and treatment.