Abstract
Abnormal mechanical stimulation contributes to articular cartilage degeneration and osteoarthritis (OA) development. Many long noncoding RNAs (lncRNAs) are involved in mechanical force-induced cartilage degeneration. LncRNA HOTAIR (HOTAIR) has been demonstrated to increase osteoarthritis progression. However, the roles of HOTAIR in mechanical stimulation-treated chondrocytes are still unclear. In this study, we found that mechanical stimulation significantly induced apoptosis in C28/I2 cells. In addition, the expression of HOTAIR was up regulated and the expression of miR-221 was down regulated. Knockdown of HOTAIR effectively ameliorated cell apoptosis induced by mechanical stimulation. HOTAIR could interact with miR-221, which targeted to degrade BBC3. Overexpression of BBC3 could reverse the decreased apoptotic rates induced by HOTAIR knockdown. Collectively, HOTAIR promoted mechanical stimulation-induced apoptosis by regulating the miR-221/BBC3 axis in C28/I2 cells.