Inhibition of miR-27a suppresses the inflammatory response via the p38/MAPK pathway in intervertebral disc cells

The current study aimed to investigate the role of miR-27a in intervertebral disc degeneration (IDD) and to examine the underlying mechanisms. Quantitative polymerase chain reaction (qPCR) was performed to detect the expression level of miR-27a in the nucleus pulposus (NP) tissues of patients with IDD, and the results revealed an increasing expression of miR-27a in IDD compared with the control. To further investigate the role of miR-27a in IDD, a stable human NP cell line with low miR-27a expression was generated by transfecting cells with a lentiviral antigomiR-27a inhibitor. In addition, a human NP cell inflammation model was established by lipopolysaccharide (LPS; 10 mu M) stimulation. The miR-27a expression in NP cells was determined by qPCR, while the expression of its target proteins; p-p38 and nuclear factor (NF-kappa B) was measured by western blot analysis. Furthermore, the mRNA and protein expression levels of proinflammatory factors, including interleukin (IL)-1 beta, IL-6 and tumor necrosis factor-alpha (TNF-alpha), were also evaluated by qPCR and ELISA, respectively. The current results confirmed that miR-27a was significantly upregulated in IDD. In vitro, downregulation of miR-27a in LPS-stimulated NP cells by transfection with the miR-27a inhibitor resulted in suppression of p-p38 and NF-kappa B expression levels. Furthermore, the production of the proinflammatory factors IL-1 beta, IL-6 and TNF-alpha was significantly reduced in LPS-stimulated NP cells with down-regulated miR-27a. In conclusion, miR-27a may function as a promoter in IDD development, while inhibition of miR-27a may suppress proinflammatory factors released by intervertebral disc cells by regulating the p38/mitogen-activated protein kinase (MAPK) signaling pathway.