MicroRNA­186­5p 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)­186­5p serves a key role in the development of various tumors, such as osteosarcoma, non­small­cell lung cancer cells, glioma and colorectal cancer. The present study aimed to investigate the effect of miR­186­5p in OA. Different concentrations of IL­1ß were used to treat the human chondrocyte cell line CHON­001 to simulate inflammation, and CHON­001 cell injury was assessed by detecting cell viability, apoptosis, caspase-3 activity and the levels of TNF­α, IL­8 and IL­6. Subsequently, reverse transcription­quantitative PCR was performed to measure miR­186­5p expression. The results demonstrated that following IL­1ß treatment, CHON­001 cell viability was suppressed, apoptosis was promoted, the caspase-3 activity was significantly enhanced and the release of TNF­α, IL­8 and IL­6 was increased. In addition, IL­1ß treatment significantly upregulated miR­186­5p expression in CHON­001 cells. It was also identified that MAPK1 was a target gene of miR­186­5p, and was negatively regulated by miR­186­5p. miR­186 inhibitor and MAPK1­small interfering RNA (siRNA) were transfected into CHON­001 cells to investigate the effect of miR­186­5p on CHON­001 cell injury induced by IL­1ß. The results demonstrated that miR­186 inhibitor suppressed the effects of IL­1ß on CHON­001 cells, and these effects were reversed by MAPK1­siRNA. In conclusion, the present results indicated that miR­186­5p could attenuate IL­1ß­induced chondrocyte inflammation damage by increasing MAPK1 expression, suggesting that miR­186­5p may be used as a potential therapeutic target for OA.