MiR-502-5p inhibits IL-1β-induced chondrocyte injury by targeting TRAF2

Osteoarthritis (OA) is characterized by articular cartilage degradation and joint inflammation. MicroRNAs have been proven to play an important role in the regulation of chondrogenesis. The aim of the present study was to investigate the effect of miR-502-5p in OA. The results showed that miR-502-5p levels were significantly down-regulated in OA articular tissues and IL-1 beta-induced chondrocytes compared with control groups. MiR-502-5p overexpression inhibited IL-1 beta-induced reduction in cell viability and increase in cell apoptosis, and alleviated IL-1 beta-induced extracellular matrix (ECM) metabolic imbalance and pro-inflammatory cytokine production. MiR-502-5p targeted the 30-untranslated region (UTR) of TRAF2 to inhibit its expression. The IL-1 beta-induced activation of NF-kappa B signaling pathway was inhibited by PDTC, an inhibitor of NF-kappa B, which was also suppressed by the miR-502-5p mimic and TRAF2 siRNA transfection. In conclusion, miR-502-5p may exhibit a protective effect on IL-1 beta-induced chondrocyte injury by targeting TRAF2 and inhibiting NF-kappa B signaling pathway. (C) 2016 Elsevier Inc. All rights reserved.