Emerging evidence has shown that microRNAs are important regulators in osteoarthritis (OA). Here, we investigated the function role of miR-455-3p in the pathogenesis of OA and the underlying molecular mechanisms. We first established the in vitro OA model using IL-1β treated human chondrocyte cell line CHON-001. Using quantitative real time PCR, we observed the expression of miR-455-3p expression was up-regulated in the OA cartilage tissues and IL-1β-treated chondrocytes. A series of function assays, including CCK-8 assay, flow cytometry, and ELISA assay showed that miR-455-3p contributed to IL-1β-induced apoptosis and inflammation. Moreover, COL2A1 was confirmed as a target of miR-455-3p by luciferase reporter assay. Furthermore, COL2A1 knockdown reversed the effects of miR-455-3p inhibition, and aggravated the effects of miR-455-3p overexpression on IL-1β-induced OA-like phenomenon. Taken together, these results revealed that miR-455-3p/COL2A1 axis might provide a novel molecular target for the treatment of OA.
Keywords: COL2A1; Osteoarthritis; apoptosis; inflammation; miR-455-3p.