The Role of miR-31-5p in the Development of Intervertebral Disc Degeneration and Its Therapeutic Potential

Intervertebral disc degeneration (IDD) refers to the abnormal response of cell-mediated progressive structural failure. In order to understand the molecular mechanism of the maintenance and destruction of the intervertebral disc, new IDD treatment methods are developed. Here, we first analyzed the k...

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Main Authors: Yong Zhou, Mingsi Deng, Jiqing Su, Wei Zhang, Dongbiao Liu, Zhengguang Wang
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-03-01
Series:Frontiers in Cell and Developmental Biology
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fcell.2021.633974/full
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author Yong Zhou
Mingsi Deng
Jiqing Su
Wei Zhang
Dongbiao Liu
Zhengguang Wang
author_facet Yong Zhou
Mingsi Deng
Jiqing Su
Wei Zhang
Dongbiao Liu
Zhengguang Wang
author_sort Yong Zhou
collection DOAJ
description Intervertebral disc degeneration (IDD) refers to the abnormal response of cell-mediated progressive structural failure. In order to understand the molecular mechanism of the maintenance and destruction of the intervertebral disc, new IDD treatment methods are developed. Here, we first analyzed the key regulators of IDD through microRNAs microarrays. Then, the level of miR-31-5p was evaluated by qRT-PCR. The association between miR-31-5p and Stromal cell-derived factor 1 (SDF-1)/CXCR7 axis was assessed by 3′-untranslated region (UTR) cloning and luciferase assay. The apoptosis of cells under different treatments was evaluated by flow cytometer. The cell proliferation was assessed by EdU assay. After IDD model establishment, the discs of mice tail were harvested for histological and radiographic evaluation in each group. Finally, the protein levels of SDF-1, CXCR7, ADAMTS-5, Col II, Aggrecan, and MMP13 were assessed by western blot. The results show that miR-31-5p is a key regulator of IDD and its level is down-regulated in IDD. Overexpression of miR-31-5p facilitates nucleus pulposus cell proliferation, inhibits apoptosis, facilitates ECM formation, and inhibits the level of matrix degrading enzymes in NP cells. The SDF-1/CXCR7 axis is the direct target of miR-31-5p. miR-31-5p acts on IDD by regulating SDF-1/CXCR7. In vitro experiments further verified that the up-regulation of miR-31-5p prevented the development of IDD. In conclusion, overexpression of miR-31-5p can inhibit IDD by regulating SDF-1/CXCR7.
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spelling doaj.art-39e2cfa7a5cf4d0a9d36e2fb772d189d2022-12-21T23:41:26ZengFrontiers Media S.A.Frontiers in Cell and Developmental Biology2296-634X2021-03-01910.3389/fcell.2021.633974633974The Role of miR-31-5p in the Development of Intervertebral Disc Degeneration and Its Therapeutic PotentialYong Zhou0Mingsi Deng1Jiqing Su2Wei Zhang3Dongbiao Liu4Zhengguang Wang5Department of Orthopaedics, The Third Xiangya Hospital of Central South University, Changsha, ChinaDepartment of Stomatology, Changsha Stomatological Hospital, Changsha, ChinaDepartment of Oncology, Changsha Central Hospital Affiliated to Nanhua University, Changsha, ChinaInstitute of Clinical Pharmacology, Central South University, Changsha, ChinaDepartment of Orthopaedics, The Third Xiangya Hospital of Central South University, Changsha, ChinaDepartment of Orthopaedics, The Third Xiangya Hospital of Central South University, Changsha, ChinaIntervertebral disc degeneration (IDD) refers to the abnormal response of cell-mediated progressive structural failure. In order to understand the molecular mechanism of the maintenance and destruction of the intervertebral disc, new IDD treatment methods are developed. Here, we first analyzed the key regulators of IDD through microRNAs microarrays. Then, the level of miR-31-5p was evaluated by qRT-PCR. The association between miR-31-5p and Stromal cell-derived factor 1 (SDF-1)/CXCR7 axis was assessed by 3′-untranslated region (UTR) cloning and luciferase assay. The apoptosis of cells under different treatments was evaluated by flow cytometer. The cell proliferation was assessed by EdU assay. After IDD model establishment, the discs of mice tail were harvested for histological and radiographic evaluation in each group. Finally, the protein levels of SDF-1, CXCR7, ADAMTS-5, Col II, Aggrecan, and MMP13 were assessed by western blot. The results show that miR-31-5p is a key regulator of IDD and its level is down-regulated in IDD. Overexpression of miR-31-5p facilitates nucleus pulposus cell proliferation, inhibits apoptosis, facilitates ECM formation, and inhibits the level of matrix degrading enzymes in NP cells. The SDF-1/CXCR7 axis is the direct target of miR-31-5p. miR-31-5p acts on IDD by regulating SDF-1/CXCR7. In vitro experiments further verified that the up-regulation of miR-31-5p prevented the development of IDD. In conclusion, overexpression of miR-31-5p can inhibit IDD by regulating SDF-1/CXCR7.https://www.frontiersin.org/articles/10.3389/fcell.2021.633974/fullIDDmiR-31-5pSDF-1/CXCR7Col IItherapeutic potential
spellingShingle Yong Zhou
Mingsi Deng
Jiqing Su
Wei Zhang
Dongbiao Liu
Zhengguang Wang
The Role of miR-31-5p in the Development of Intervertebral Disc Degeneration and Its Therapeutic Potential
Frontiers in Cell and Developmental Biology
IDD
miR-31-5p
SDF-1/CXCR7
Col II
therapeutic potential
title The Role of miR-31-5p in the Development of Intervertebral Disc Degeneration and Its Therapeutic Potential
title_full The Role of miR-31-5p in the Development of Intervertebral Disc Degeneration and Its Therapeutic Potential
title_fullStr The Role of miR-31-5p in the Development of Intervertebral Disc Degeneration and Its Therapeutic Potential
title_full_unstemmed The Role of miR-31-5p in the Development of Intervertebral Disc Degeneration and Its Therapeutic Potential
title_short The Role of miR-31-5p in the Development of Intervertebral Disc Degeneration and Its Therapeutic Potential
title_sort role of mir 31 5p in the development of intervertebral disc degeneration and its therapeutic potential
topic IDD
miR-31-5p
SDF-1/CXCR7
Col II
therapeutic potential
url https://www.frontiersin.org/articles/10.3389/fcell.2021.633974/full
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