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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,...

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Autores principales: Wang, Xuesong, Peng, Lei, Gong, Xiaojin, Zhang, Xiugong, Sun, Ruifu, Du, Jinlong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6201218/
https://www.ncbi.nlm.nih.gov/pubmed/30156374
http://dx.doi.org/10.1111/jcmm.13817
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author Wang, Xuesong
Peng, Lei
Gong, Xiaojin
Zhang, Xiugong
Sun, Ruifu
Du, Jinlong
author_facet Wang, Xuesong
Peng, Lei
Gong, Xiaojin
Zhang, Xiugong
Sun, Ruifu
Du, Jinlong
author_sort Wang, Xuesong
collection PubMed
description 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.
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spelling pubmed-62012182018-11-01 LncRNA‐RMRP promotes nucleus pulposus cell proliferation through regulating miR‐206 expression Wang, Xuesong Peng, Lei Gong, Xiaojin Zhang, Xiugong Sun, Ruifu Du, Jinlong J Cell Mol Med Original Articles 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. John Wiley and Sons Inc. 2018-08-29 2018-11 /pmc/articles/PMC6201218/ /pubmed/30156374 http://dx.doi.org/10.1111/jcmm.13817 Text en © 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Wang, Xuesong
Peng, Lei
Gong, Xiaojin
Zhang, Xiugong
Sun, Ruifu
Du, Jinlong
LncRNA‐RMRP promotes nucleus pulposus cell proliferation through regulating miR‐206 expression
title LncRNA‐RMRP promotes nucleus pulposus cell proliferation through regulating miR‐206 expression
title_full LncRNA‐RMRP promotes nucleus pulposus cell proliferation through regulating miR‐206 expression
title_fullStr LncRNA‐RMRP promotes nucleus pulposus cell proliferation through regulating miR‐206 expression
title_full_unstemmed LncRNA‐RMRP promotes nucleus pulposus cell proliferation through regulating miR‐206 expression
title_short LncRNA‐RMRP promotes nucleus pulposus cell proliferation through regulating miR‐206 expression
title_sort lncrna‐rmrp promotes nucleus pulposus cell proliferation through regulating mir‐206 expression
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6201218/
https://www.ncbi.nlm.nih.gov/pubmed/30156374
http://dx.doi.org/10.1111/jcmm.13817
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