The long non‐coding RNA maternally expressed 3‐micorRNA‐15a‐5p axis is modulated by melatonin and prevents nucleus pulposus cell inflammation and apoptosis

Abstract

AbstractNucleus pulposus (NP) cell apoptosis is regarded as a critical risk factor for intervertebral disc degeneration (IVDD). Melatonin exerts a protective role on NP cells. The study concentrates on the role and mechanism of lncRNA MEG3 in melatonin‐mediated effects on NP cells. An in vitro IVDD model was constructed using IL‐1β on human NP cells. qRT‐PCR investigated MEG3, miR‐15a‐5p and PGC‐1α mRNA levels in tissues and NP cells. IL‐1β‐treated NP cells subsequent to transfection, followed by melatonin treatment. NP cell proliferation, viability, apoptosis and inflammatory reactions were assayed. Western blot checked the profiles of PGC‐1α, SIRT1 and NF‐κB p65. Student's t‐test or one‐way analysis of variance (ANOVA) followed by Tukey's test was used for statistical tests. As indicated by the data, melatonin weakened NP cell inflammation and apoptosis and enhanced MEG3 expression. MEG3 expression was attenuated in IVDD tissues. MEG3 knockdown impaired the function of melatonin, which was, however, strengthened by miR‐15a‐5p knockdown. MEG3 targeted miR‐15a‐5p, which targeted PGC‐1α and repressed the PGC‐1α/SIRT1 pathway. Collectively, this study has disclosed that the MEG3‐miR‐15a‐5p‐PGC‐1α/SIRT1 pathway modulated by melatonin can hamper NP cell apoptosis and inflammation elicited by IL‐1β.