LncRNA HOTAIR suppresses TNF-α induced apoptosis of nucleus pulposus cells by regulating miR-34a/Bcl-2 axis

Abstract Objective The aim of this study was to investigate the regulation mechanism of HOTAIR on nucleus pulposus cell (NPC) apoptosis induced by inflammatory cytokines. Methods QRT-PCR was performed to analyze the expression of HOTAIR and miR-34a. Safranin O staining and immunohistochemical staining were measured to identify NPCs. ELISA assay was used to detect TNF-α level. Apoptosis was detected with TUNEL assay. Western blotting was measured to analyze the expression of caspase-3, Bax and Bcl-2. TargetScan was used to predict potential targets of miR-34a. Results HOTAIR was significantly low-expressed in degenerative nucleus pulposus (NP) tissues and cells of IDD patients, overexpressing HOTAIR obviously inhibited TNF-α level, NPCs apoptosis and the expression of caspase-3 and Bax, while promoted the expression of Bcl-2. MiR-34a was obviously expressed in degenerative NP tissues and cells of IDD patients. HOTAIR reduced miR-34a induced apoptosis. Apoptotic inhibition gene Bcl-2 is the target gene of miR-34a, and showed a negative relationship with miR-34a. Conclusion Our data suggest that lncRNA HOTAIR suppresses TNF-α induced NPCs apoptosis by regulating miR-34a/Bcl-2 axis in IDD patients.