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

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.