Microrna-186-5p Downregulation Inhibits Osteoarthritis Development By Targeting Mapk1

As a chronic degenerative joint disease, the characteristics of osteoarthritis (OA) are degeneration of articular cartilage, subchondral bone sclerosis and bone hyperplasia. It has been reported that microRNA (miR)-186-5p serves a key role in the development of various tumors, such as osteosarcoma, non-small-cell lung cancer cells, glioma and colorectal cancer. The present study aimed to investigate the effect of miR-186-5p in OA. Different concentrations of IL-1 beta were used to treat the human chondrocyte cell line CHON-001 to simulate inflammation, and CHON-001 cell injury was assessed by detecting cell viability, apoptosis, caspase-3 activity and the levels of TNF-alpha, IL-8 and IL-6. Subsequently, reverse transcription-quantitative PCR was performed to measure miR-186-5p expression. The results demonstrated that following IL-1 beta treatment, CHON-001 cell viability was suppressed, apoptosis was promoted, the caspase-3 activity was significantly enhanced and the release of TNF-alpha, IL-8 and IL-6 was increased. In addition, IL-1 beta treatment significantly upregulated miR-186-5p expression in CHON-001 cells. It was also identified that MAPK1 was a target gene of miR-186-5p, and was negatively regulated by miR-186-5p. miR-186 inhibitor and MAPK1-small interfering RNA (siRNA) were transfected into CHON-001 cells to investigate the effect of miR-186-5p on CHON-001 cell injury induced by IL-1 beta. The results demonstrated that miR-186 inhibitor suppressed the effects of IL-1 beta on CHON-001 cells, and these effects were reversed by MAPK1-siRNA. In conclusion, the present results indicated that miR-186-5p could attenuate IL-1 beta-induced chondrocyte inflammation damage by increasing MAPK1 expression, suggesting that miR-186-5p may be used as a potential therapeutic target for OA.