Role of the ciRS-7/miR-7 axis in the regulation of proliferation, apoptosis and inflammation of chondrocytes induced by IL-1β

Abstract

Osteoarthritis (OA) is a degenerative joint disease caused by articular cartilage degradation and joint inflammation, with considerable involvement of microRNAs and circular RNAs. However, the precise role of the ciRS-7/miR-7 axis within OA still requires further elucidation. In this study, quantitative reverse-transcription PCR (qRT-PCR) was utilized to determine the relative expression of ciRS-7 and miR-7 in blood samples from OA patients compared with those from healthy individuals. Human OA chondrocytes (C28/12 cell line) were transfected with ciRS-7-siRNA, ciRS-7-cDNA, inhibitor or miR-7 mimic to investigate the influence of ciRS-7/miR-7 expression on chondrocyte apoptosis, inflammation and related signaling pathways. Decreased ciRS-7 expression and increased miR-7 expression were observed in OA blood samples. IL-1β exposure of chondrocytes significantly inhibited proliferation and promoted inflammatory cytokine release. ciRS-7 was down-regulated but miR-7 was up-regulated in IL-1β-induced chondrocytes. Transfection of ciRS-7 siRNA and miR-7 mimic enhanced the impact of IL-1β on inflammatory cytokine release and cell apoptosis as quantified using ELISA and flow cytometry. Conversely, ciRS-7 cDNA and miR-7 inhibitor induced the reverse effect. These findings demonstrate that the ciRS-7/miR-7 axis can possibly serve as a regulator in mediating proliferation, apoptosis and inflammation in chondrocytes in the process of OA development.