Abstract
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.
Highlights
We first measured the expression of RMRP in the intervertebral disc tissues and we found 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
We showed that RMRP expression was up‐regulated in degenerated NP tissues compared to normal NP samples and RMRP expression was associated with the disc degeneration grade
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 early disc degeneration grade
Summary
Chronic low back pain (LBP) influenced more than 70% people at some time in their lives, with about 10% people becoming chronic disabled.[1,2,3] The aetiology of LBP is considered to be multifactorial, and intervertebral disc degenerative (IDD) contributes to the development of LBP.[3,4,5] The cause of IDD is thought to associate with many aetiological factors such as ageing, lifestyle and genetic predisposition.[6,7,8,9] Recent research in cell molecular biology may contemplate treating intervertebral disc itself at the molecular biology level to delay or prevent the development of IDD.[10,11,12,13,14,15] the underlying molecular and cellular mechanism of IDD progression is still unknown. | 5469 found to play important roles in diverse human diseases and biological processes.[16,17,18,19,20,21] Mounting evidence has suggested that many lncRNAs are beregulated in diverse diseases such as tumours, diabetes, coronary heart disease, osteoarthritis and IDD.[22,23,24,25,26,27,28,29] For example, Lan and colleagues[30] profiled lncRNA expression in degenerate disc tissues and normal adults’ lumbar discs by microarray and found a total of 3081 differentially expressed lncRNAs. Wang et al[31] showed that knockdown of RP11‐296A18.3 suppressed human NP cell proliferation and decreased the expression of collagen I and matrix metalloproteinase (MMP)‐13. Tan et al[32] studied the role of SNHG1 in the pathogenesis of IDD They indicated that the expression of SNHG1 was up‐regulated in the IDD samples compared to the control samples. Feng et al[33] showed that RMRP expression was up‐regulated in glioma samples compared to normal brain samples. We first measured the expression of RMRP in the intervertebral disc tissues and we found 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
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