Up-regulation of circulating microRNA-17 is associated with lumbar radicular pain following disc herniation

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Abstract

Background

Previous studies suggest that regulatory microRNAs (miRs) may modulate neuro-inflammatory processes. The purpose of the present study was to examine the role of miR-17 following intervertebral disc herniation.

Methods

In a cohort of 97 patients with leg pain and disc herniation verified on MRI, we investigated the association between circulating miR-17 and leg pain intensity. A rat model was used to examine possible changes in miR-17 expression in nucleus pulposus (NP) associated with leak of NP tissue out of the herniated disc. The functional role of miR-17 was addressed by transfection of miR-17 into THP-1 cells (human monocyte cell line).

Results

An association between the level of miR-17 in serum and the intensity of lumbar radicular pain was shown. Up-regulation of miR-17 in the rat NP tissue when applied onto spinal nerve roots and increased release of TNF following transfection of miR-17 into THP-1 cells were also observed. Hence, our data suggest that miR-17 may be involved in the pathophysiology underlying lumbar radicular pain after disc herniation.

Conclusions

We conclude that miR-17 may be associated with the intensity of lumbar radicular pain after disc herniation, possibly through a TNF-driven pro-inflammatory mechanism.

Electronic supplementary material

The online version of this article (10.1186/s13075-019-1967-y) contains supplementary material, which is available to authorized users.

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Most cited references 53

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Altered expression of MicroRNA in synovial fibroblasts and synovial tissue in rheumatoid arthritis.

Joanna Stanczyk, Deena Pedrioli, Fabia Brentano … (2008)

MicroRNAs (miRNA) have recently emerged as a new class of modulators of gene expression. In this study we investigated the expression, regulation, and function of miR-155 and miR-146a in rheumatoid arthritis (RA) synovial fibroblasts (RASFs) and RA synovial tissue. Locked nucleic acid microarray was used to screen for differentially expressed miRNA in RASFs treated with tumor necrosis factor alpha (TNFalpha). TaqMan-based real-time polymerase chain reaction was applied to measure the levels of miR-155 and miR-146a. Enforced overexpression of miR-155 was used to investigate the function of miR-155 in RASFs. Microarray analysis of miRNA expressed in RASFs treated with TNFalpha revealed a prominent up-regulation of miR-155. Constitutive expression of both miR-155 and miR-146a was higher in RASFs than in those from patients with osteoarthritis (OA), and expression of miR-155 could be further induced by TNFalpha, interleukin-1beta, lipopolysaccharide, poly(I-C), and bacterial lipoprotein. The expression of miR-155 in RA synovial tissue was higher than in OA synovial tissue. Enforced expression of miR-155 in RASFs was found to repress the levels of matrix metalloproteinase 3 (MMP-3) and reduce the induction of MMPs 3 and 1 by Toll-like receptor ligands and cytokines. Moreover, compared with monocytes from RA peripheral blood, RA synovial fluid monocytes displayed higher levels of miR-155. This study provides the first description of increased expression of miRNA miR-155 and miR-146a in RA. Based on these findings, we postulate that the inflammatory milieu may alter miRNA expression profiles in resident cells of the rheumatoid joints. Considering the repressive effect of miR-155 on the expression of MMPs 3 and 1 in RASFs, we hypothesize that miR-155 may be involved in modulation of the destructive properties of RASFs.

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Establishment and characterization of a human acute monocytic leukemia cell line (THP-1).

M Yamabe, K Tada, Y. Yamaguchi … (1980)

A human leukemic cell line (THP-1) cultured from the blood of a boy with acute monocytic leukemia is described. This cell line had Fc and C3b receptors, but no surface or cytoplasmic immunoglobulins. HLA haplotypes of THP-1 were HLA-A2, -A9, -B5, -DRW1 and -DRW2. The monocytic nature of the cell line was characterized by: (1) the presence of alpha-naphthyl butyrate esterase activities which could be inhibited by NaF; (2) lysozyme production; (3) the phagocytosis of latex particles and sensitized sheep erythrocytes; and (4) the ability to restore T-lymphocyte response to Con A. The cells did not possess Epstein-Barr virus-associated nuclear antigen. These results indicate that THP-1 is a leukemia cell line with distinct monocytic markers. During culture, THP-1 maintained these monocytic characteristics for over 14 months.

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MicroRNAs 17-5p-20a-106a control monocytopoiesis through AML1 targeting and M-CSF receptor upregulation.

Cesare Peschle, Ercole Brunetti, Elvira Pelosi … (2007)

We investigated the role of microRNAs (miRNA) 17-5p, 20a and 106a in monocytic differentiation and maturation. In unilineage monocytic culture generated by haematopoietic progenitor cells these miRNAs are downregulated, whereas the transcription factor acute myeloid leukaemia-1 (AML1; also known as Runt-related transcription factor 1, Runx1) is upregulated at protein but not mRNA level. As miRNAs 17-5p, 20a and 106a bind the AML1 mRNA 3'UTR, their decline may unblock AML1 translation. Accordingly, transfection with miRNA 17-5p-20a-106a suppresses AML1 protein expression, leading to M-CSF receptor (M-CSFR) downregulation, enhanced blast proliferation and inhibition of monocytic differentiation and maturation. Treatment with anti-miRNA 17-5p, 20a and 106a causes opposite effects. Knockdown of AML1 or M-CSFR by short interfering RNA (siRNA) mimics the action of the miRNA 17-5p-20a-106a, confirming that these miRNAs target AML1, which promotes M-CSFR transcription. In addition, AML1 binds the miRNA 17-5p-92 and 106a-92 cluster promoters and transcriptionally inhibits the expression of miRNA 17-5p-20a-106a. These studies indicate that monocytopoiesis is controlled by a circuitry involving sequentially miRNA 17-5p-20a-106a, AML1 and M-CSFR, whereby miRNA 17-5p-20a-106a function as a master gene complex interlinked with AML1 in a mutual negative feedback loop.

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Author and article information

Contributors

Eivind Hasvik:

ORCID: http://orcid.org/0000-0001-8770-5019

eivind.hasvik@so-hf.no

Tiril Schjølberg: tiril.schjolberg@stami.no

Daniel Pitz Jacobsen: danielpitz.jacobsen@stami.no

Anne Julsrud Haugen: anne.julsrud.haugen@so-hf.no

Lars Grøvle: lars.grovle@so-hf.no

Elina Iordanova Schistad: uxioel@ous-hf.no

Johannes Gjerstad: johannes.gjerstad@stami.no

Journal

Journal ID (nlm-ta): Arthritis Res Ther

Journal ID (iso-abbrev): Arthritis Res. Ther

Title: Arthritis Research & Therapy

Publisher: BioMed Central (London )

ISSN (Print): 1478-6354

ISSN (Electronic): 1478-6362

Publication date (Electronic): 13 August 2019

Publication date PMC-release: 13 August 2019

Publication date (Print): 2019

Volume: 21

Electronic Location Identifier: 186

Affiliations

[1 ]GRID grid.412938.5, Department of Physical Medicine and Rehabilitation, , Østfold Hospital Trust, ; Grålum, Norway

[2 ]ISNI 0000 0004 0630 3985, GRID grid.416876.a, Department of Work Psychology and Physiology, , National Institute of Occupational Health, ; Oslo, Norway

[3 ]GRID grid.412938.5, Department of Rheumatology, , Østfold Hospital Trust, ; Grålum, Norway

[4 ]ISNI 0000 0004 0389 8485, GRID grid.55325.34, Department of Physical Medicine and Rehabilitation, , Oslo University Hospital, ; Ullevål, Norway

Author information

Eivind Hasvik http://orcid.org/0000-0001-8770-5019

Article

Publisher ID: 1967

DOI: 10.1186/s13075-019-1967-y

PMC ID: 6693234

PubMed ID: 31409426

SO-VID: d7056a5f-5467-44bb-920c-1c40548d654b

License:

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License ( http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver ( http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

History

Date received : 20 November 2018

Date accepted : 25 July 2019

Custom metadata

ScienceOpen disciplines: Orthopedics

Keywords: microrna-17,disc herniation,nucleus pulposus,lumbar radicular pain,radiculopathy,low back-related leg pain,inflammation,tnf,monocytes,macrophages

Data availability:

ScienceOpen disciplines: Orthopedics

Keywords: microrna-17, disc herniation, nucleus pulposus, lumbar radicular pain, radiculopathy, low back-related leg pain, inflammation, tnf, monocytes, macrophages

Up-regulation of circulating microRNA-17 is associated with lumbar radicular pain following disc herniation

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Most cited references 53

Altered expression of MicroRNA in synovial fibroblasts and synovial tissue in rheumatoid arthritis.

Establishment and characterization of a human acute monocytic leukemia cell line (THP-1).

MicroRNAs 17-5p-20a-106a control monocytopoiesis through AML1 targeting and M-CSF receptor upregulation.

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