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.

Intervertebral disc degeneration (IDD) is a major cause of lower back pain. The high morbidity associated with this disease diminishes the quality of life of those who are affected. MicroRNAs (miRs) play crucial roles in various diseases, including IDD. However, the mechanism via which miR-200c-3p plays a role in the development of IDD remains unknown. The present study aimed to investigate the effect of miR-200c-3p on the progression of IDD and the underlying mechanism. The expression level of miR-200c-3p was evaluated in intervertebral disc tissues from patients with IDD. To construct the IDD cell model, the nucleus pulposus (NP) cells were treated with lipopolysaccharide (LPS) 24 h following transfection with miR-200c-3p mimic or inhibitor. A luciferase activity assay was performed, while reverse transcription-quantitative PCR and western blotting were conducted to determine the RNA and protein expression levels, respectively. The expression level of miR-200c-3p in the intervertebral disc tissues of patients with IDD was lower than that of normal subjects. LPS treatment reduced the expression level of miR-200c-3p in NP cells. Moreover, miR-200c-3p mimic inhibited LPS-induced NP cell apoptosis. It was found that miR-200c-3p attenuated inflammatory cytokine levels and extracellular matrix (ECM) degradation in NP cells. Furthermore, miR-200c-3p targeted Ras-related protein 2C (RAP2C) in NP cells. RAP2C promoted apoptosis, inflammatory cytokine levels and ECM degradation by activating ERK signaling. Knockdown of RAP2C and inhibition of ERK signaling by SCH772984 partially reversed the proinflammatory effect of the miR-200c-3p inhibitor on LPS-treated NP cells. Thus, miR-200c-3p inhibits NP cell apoptosis, inflammatory cytokine levels and ECM degradation in IDD by targeting RAP2C/ERK signaling.

Background: Osteoarthritis (OA) is a joint disease characterized by progressive cartilage degradation and inflammation, but the detailed pathogenesis of OA is still unclear. Here, we aimed to investigate the role of LincRNA-Cox2 in OA progression and the potential mechanism.Methods: OA mouse model and IL-1β-induced injury of mouse chondrocytes were conducted. Si-Cox2 was transfected into chondrocytes for elucidating the effect of LincRNA-Cox2 on OA. qR-TPCR was used to detect the expression of LincRNA-Cox2 and miR-150. Cell proliferation and apoptosis were analyzed by MTT assay and Annexin V/PI stain respectively. Western blot was used to evaluate the protein levels in chondrocytes.Results: High levels of LincRNA-Cox2 were observed in both cartilage tissues of OA and IL-1β-treated chondrocytes. Knockdown of LincRNA-Cox2 promoted the proliferation and inhibited apoptosis of chondrocytes. Mechanically, LincRNA-Cox2 directly target to miR-150, acting as a ceRNA, and the effect of si-Cox2 on proliferation and apoptosis in chondrocytes was reversed by miR-150 inhibitor. Moreover, LincRNA-Cox2 had ability to activate wnt/β-catenin pathway to regulate chondrocytes proliferation and apoptosis.Conclusion: Silencing LincRNA-Cox2 plays a protective role in OA by enhancing the proliferation and suppressing apoptosis of chondrocytes, which was related with increase of miR-150 and activation of Wnt/β-catenin pathway.