LncRNA-RMRP promotes nucleus pulposus cell proliferation through regulating miR-206 expression.

Long noncoding RNAs (LncRNAs) are involved in the pathogenesis of intervertebral disc degeneration (IDD). However, the biological function and expression of RMRP were still unclear. In our study, we showed that RMRP expression was up-regulated in degenerated NP tissues compared to normal NP samples, and higher RMRP expression was associated with the disc degeneration grade. Further studies indicated that ectopic expression of RMRP enhanced NP cell growth and also enhanced the expression of ki-67, PCNA and cyclin D1 in the NP cell. Moreover, overexpression of RMRP promoted the expression of Type II collagen and aggrecan and suppressed the expression of MMP13 and ADAMTS4. In addition, we found that the expression of miR-206 was down-regulated in degenerated NP tissues compared to normal NP samples, and lower miR-206 expression was correlated with the disc degeneration grade. Interestingly, we indicated that miR-206 expression in NP tissues was negatively correlated with the expression of RMRP. Ectopic expression of miR-206 suppressed NP cell proliferation and suppressed the expression of Type II collagen and aggrecan and enhanced the expression of MMP13 and ADAMTS4. Furthermore, we demonstrated that overexpression of RMRP increased NP cell growth and regulated ECM expression through targeting miR-206. These results suggested that lncRNA-RMRP promoted the progression of IDD through targeting miR-206, providing an attractive new therapeutic approach for the treatment of IDD disease.