lncRNA-CIR regulates cell apoptosis of chondrocytes in osteoarthritis

Background and Objectives Osteoarthritis (OA) is a complex chronic degenerative joint disease involving oxidative stress, inflammation, and apoptosis of chondrocytes. As decoys of micro RNAs, long non-coding RNAs (lncRNAs) play important roles in various biological processes. This study was designed to investigate the interactions between lncRNA-CIR, chondrocyte apoptosis, and the molecular mechanisms underlying OA. Methods Primary cultured chondrocytes were stressed using H2O2, IL-1 beta, or TNF-& to simulate conditions found in OA. Quantitative real-time PCR was performed to detect miR-130a, lncRNA-CIR, and Bim mRNA expression levels. Western blot analysis was used to detect Bim protein expression levels. Reactive oxygen species (ROS) levels were assayed by detecting the fluorescent signal of 2 ',7 '-dichlorodihydrofluorescein diacetate (DCFH-DA). Cell apoptosis was measured with combined staining of PI and DAPI. lncRNA-CIR knockdown and miR-130a over-expression or inhibition were performed using small interfering RNAs, and miR-130 mimics or inhibitors, respectively. Results lncRNA-CIR is significantly upregulated in OA patients, accompanied by downregulation of miR-130a and upregulation of Bim. Bio-informatics analysis predicted miR-130a as a target of both lncRNA-CIR and Bim. While lncRNA-CIR knockdown significantly increased the expression of Bim, miR-130a significantly suppressed Bim expression, with accompanying increases of ROS level, inflammatory mediator release, cell apoptosis, and relative luciferase activity. Conclusions The present findings demonstrated that the lncRNA-CIR/miR-130a/Bim axis is involved in oxidative stress-related apoptosis of chondrocytes in OA.