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‑1β 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‑α, IL‑8 and IL‑6. Subsequently, reverse transcription‑quantitative PCR was performed to measure miR‑186‑5p expression. The results demonstrated that following IL‑1β treatment, CHON‑001 cell viability was suppressed, apoptosis was promoted, the caspase-3 activity was significantly enhanced and the release of TNF‑α, IL‑8 and IL‑6 was increased. In addition, IL‑1β 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‑1β. The results demonstrated that miR‑186 inhibitor suppressed the effects of IL‑1β 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‑1β‑induced chondrocyte inflammation damage by increasing MAPK1 expression, suggesting that miR‑186‑5p may be used as a potential therapeutic target for OA.