LncRNA HOTAIR modulates chondrocyte apoptosis and inflammation in osteoarthritis via regulating miR‐1277‐5p/SGTB axis

Abstract Osteoarthritis (OA) is a common degenerative joint disease in the elderly. This study aimed to investigate the role and mechanism of lncRNA HOX transcript antisense RNA (HOTAIR) in lipopolysaccharide (LPS)‐treated chondrocytes in OA. CHON‐001 chondrocytes treated with LPS were used as a cell model of OA. The levels of HOTAIR, miR‐1277‐5p and small glutamine rich tetratricopeptide repeat containing beta (SGTB) were measured via quantitative real‐time polymerase chain reaction or western blot. Cell viability and apoptosis were assessed using Cell Counting Kit‐8 and flow cytometry. The levels of inflammation‐related factors were examined via enzyme‐linked immunosorbent assay (ELISA). Aggrecan and Collagen II protein levels were detected using western blot. The interaction among HOTAIR, miR‐1277‐5p and SGTB were validated by dual‐luciferase reporter analysis. HOTAIR and SGTB were up‐regulated, while miR‐1277‐5p was down‐regulated in OA cartilages and LPS‐stimulated CHON‐001 chondrocytes. HOTAIR depletion inhibited LPS‐induced apoptosis and inflammation in chondrocytes. Moreover, down‐regulation of HOTAIR attenuated LPS‐triggered chondrocyte apoptosis and inflammation via sponging miR‐1277‐5p. Also, miR‐1277‐5p repressed LPS‐induced chondrocyte apoptosis and inflammation by targeting SGTB. Furthermore, HOTAIR enhanced SGTB expression by sponging miR‐1277‐5p. HOTAIR aggravated chondrocyte apoptosis and inflammation in OA via regulating miR‐1277‐5p/SGTB pathway.