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Role of miR-155 in the regulation of MMP-16 expression in intervertebral disc degeneration
Wei-Lin Zhang1,2, Yu-Fei Chen3, Hong-Zheng Meng1
1Department of Orthopedics, The First Hospital of China Medical University, 155 North Nanjing Street, Shenyang 110001, Liaoning, China.
Abstract:
The molecular mechanisms of intervertebral disc degeneration (IDD) remain elusive. We found that miR-155 is down-regulated in degenerative nucleus pulposus (NP), and more severe degeneration is correlated with higher matrix metallopeptidase 16 (MMP-16) expression. MMP-16 also degraded matrix aggrecan. Here, we addressed the in vivo miR-155-mediated pathological impact on IDD using a classic puncture mouse model. Lentiviral upregulated-miR-155 or downregulated-miR-155 was transduced into the discs of C57 mice, which was validated by real-time polymerase chain reaction (real-time PCR) and in situ hybridization. Immunohistochemistry and western blotting revealed that up-regulation of miR-155 resulted in down-regulation of MMP-16 and an increase in aggrecan and collagen type II in mouse NP; whereas, down-regulation of miR-155 resulted in up-regulation of MMP-16 and a decrease in aggrecan in mouse NP. Radiographic and histological analysis showed that the up-regulation of miR-155 attenuated IDD, while down-regulation of miR-155 resulted in the deterioration of IDD. These findings indicate that decreased miR-155 contributed to the up-regulation of MMP-16 in vivo, and MMP-16 further degraded aggrecan and collagen type II, leading to the dehydration and degeneration of discs. Our findings revealed a therapeutic role for miR-155 in IDD. © 2017 The Authors. Journal of Orthopaedic Research Published by Wiley Periodicals, Inc. on behalf of Orthopaedic Research Society. J Orthop Res 35:1323-1334, 2017.
Insights
MicroRNA-155 (miR-155) deficiency exacerbates intervertebral disc degeneration (IDD) by increasing matrix metallopeptidase 16 (MMP-16) and degrading disc matrix. Restoring miR-155 levels may offer a therapeutic strategy for IDD.
Area of Science:
- Biochemistry
- Molecular Biology
- Orthopedics
Background:
- Intervertebral disc degeneration (IDD) is a complex process with poorly understood molecular underpinnings.
- MicroRNA-155 (miR-155) is downregulated in degenerative nucleus pulposus (NP).
- Matrix metallopeptidase 16 (MMP-16) expression correlates with IDD severity and degrades aggrecan.
Purpose of the Study:
- To investigate the in vivo role of miR-155 in intervertebral disc degeneration.
- To elucidate the molecular mechanism linking miR-155, MMP-16, and disc matrix degradation.
Main Methods:
- A mouse model of IDD was established using puncture.
- Lentiviral vectors were used to upregulate or downregulate miR-155 in mouse intervertebral discs.
- Real-time PCR, in situ hybridization, immunohistochemistry, western blotting, radiographic, and histological analyses were performed.
Main Results:
- Upregulation of miR-155 decreased MMP-16 expression and increased aggrecan and collagen type II levels in NP.
- Downregulation of miR-155 increased MMP-16 expression and decreased aggrecan levels in NP.
- miR-155 upregulation attenuated IDD, while downregulation exacerbated it.
Conclusions:
- Decreased miR-155 contributes to IDD by upregulating MMP-16, which degrades disc matrix components.
- MMP-16-mediated degradation leads to disc dehydration and degeneration.
- miR-155 demonstrates a potential therapeutic role in treating intervertebral disc degeneration.
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