miR-455-3p enhances chondrocytes apoptosis and inflammation by targeting COL2A1 in the in vitro osteoarthritis model

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-1 beta 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-1 beta-treated chondrocytes. A series of function assays, including CCK-8 assay, flow cytometry, and ELISA assay showed that miR-455-3p contributed to IL-1 beta-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-1 beta-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.