MicroRNA-107 regulates autophagy and apoptosis of osteoarthritis chondrocytes by targeting TRAF3.

Osteoarthritis (OA) is a degenerative joint disease with characteristics of reduced cartilage cellularity, subchondral sclerosis and synoviti. Ultrasonic diagnosis plays pivotal role in diagnosing OA in the clinical, while biological markers are equal important to the diagnosis of OA. This study aimed to identify and characterize a biomarker, the expression of microRNA-107 (miR-107) in normal and OA chondrocytes, and to explore its effect on OA pathogenesis. Transfection with miR-107 mimic or inhibitor was used to investigate the effect of miR-107 on OA chondrocytes and to identify miR-107 target. Activation of AKT, mTOR and P65 was evaluated by Western blot analysis. Chondrocyte apoptosis was detected by using flow cytometer. Our results showed that the expression level of miR-107 in OA chondrocytes was obviously lower than control chondrocytes. Overexpression of miR-107 inhibited apoptosis and promoted autophagy in OA chondrocytes. Additionally, overexpression of miR-107 inhibited the activation of AKT/mTOR and NF-κB pathway by targeting TRAF3 genes. In vivo analysis revealed that miR-107 was also lowly expressed in rats with OA, and its abnormal expression significantly affected cell apoptosis. In conclusion, miR-107 regulated apoptosis and autophagy of OA chondrocytes by targeting TRAF3, and it might be used as a potential target for OA therapy.