Role of lincRNA-Cox2 targeting miR-150 in regulating the viability of chondrocytes in osteoarthritis.

Abstract

Osteoarthritis (OA) is a joint disease characterised by progressive cartilage degradation and inflammation, but the detailed pathogenesis of OA remains unclear. The present study aimed to investigate the role of long intergenic non-coding RNA (lincRNA)-Cox2 in OA progression and the potential mechanism. An OA mouse model was used for in vivo experiments, and IL-1β-induced injury of mouse chondrocytes was conducted for in vitro experiments. Small interfering (si)-Cox2 was transfected into chondrocytes to elucidate the effect of lincRNA-Cox2 on OA. Quantitative reverse transcription PCR assays were conducted to detect the expression of lincRNA-Cox2 and microRNA (miR)-150. Cell proliferation and apoptosis were analysed based on an MTT assay and annexin V/propidium iodide staining, respectively. Western blotting was performed to evaluate the protein expression levels of Ki-67, PCNA, Bax, cleaved (c)-Caspase-3, c-Caspase-9 and Wnt/β-catenin pathway-associated proteins in chondrocytes. High levels of lincRNA-Cox2 were observed in cartilage tissues of the OA mouse model in vivo. In the in vitro experiments, the expression of lincRNA-Cox2 was increased in IL-1β-treated chondrocytes. Knockdown of lincRNA-Cox2 promoted the proliferation and inhibited the apoptosis of chondrocytes. Mechanistically, lincRNA-Cox2 was found to directly target miR-150, acting as a competing endogenous RNA, and the effect of si-Cox2 on the proliferation and apoptosis of chondrocytes was reversed by miR-150 inhibitors. Moreover, lincRNA-Cox2 activated the Wnt/β-catenin pathway to regulate chondrocyte proliferation and apoptosis. The present study demonstrated that silencing lincRNA-Cox2 expression plays a protective role in OA by enhancing the proliferation and suppressing the apoptosis of chondrocytes, which is related to increased miR-150 expression and activation of the Wnt/β-catenin pathway.