Evidence map›Paper›PMID 25311550›Full record

ArticleGene2015

MicroRNA-146a reduces IL-1 dependent inflammatory responses in the intervertebral disc.

Su-Xi Gu, Xin Li, John L Hamilton, Ana Chee, Ranjan Kc, Di Chen, Howard S An, Jae-Sung Kim, Chun-do Oh, Yuan-Zheng Ma and 2 more

Abstract read
In one paragraph

Article in Gene, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

58 citing papers in PubMed, 96 citations in OpenAlex.

  1. Trial
  2. Review
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  5. Article
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  7. Review
  8. Review
  9. Review
  10. Article
  11. Mechanobiology of MicroRNAs in Intervertebral Disk Degeneration.Journal of spine research and surgery · 2023
    Article
  12. Review
  13. Article
  14. Article
  15. Role of microRNAs in intervertebral disc degeneration (Review).Experimental and therapeutic medicine · 2021
    Review
  16. Review
  17. Article
  18. Article
  19. Review
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors at 4 institutions in 3 countries.

Su-Xi GuDepartment of Biochemistry, Rush University Medical Center, Chicago, IL 60612, USA; Department of Orthopedic Surgery, Rush University Medical Center, Chicago, IL 60612, USA; Department of Orthopedic Surgery, PLA309 Hospital, Beijing 100091, China.
Xin LiDepartment of Biochemistry, Rush University Medical Center, Chicago, IL 60612, USA.
John L HamiltonDepartment of Biochemistry, Rush University Medical Center, Chicago, IL 60612, USA.
Ana CheeDepartment of Orthopedic Surgery, Rush University Medical Center, Chicago, IL 60612, USA.
Ranjan KcDepartment of Biochemistry, Rush University Medical Center, Chicago, IL 60612, USA.
Di ChenDepartment of Biochemistry, Rush University Medical Center, Chicago, IL 60612, USA.
Howard S AnDepartment of Orthopedic Surgery, Rush University Medical Center, Chicago, IL 60612, USA.
Jae-Sung KimThe Division of Natural Medical Sciences, College of Health Science, Chosun University, Gwangju 501-759, Republic of Korea.
Chun-do OhDepartment of Biochemistry, Rush University Medical Center, Chicago, IL 60612, USA.
Yuan-Zheng MaDepartment of Orthopedic Surgery, PLA309 Hospital, Beijing 100091, China. Electronic address: 309mayuanzheng@gmail.com.
Andre J van WijnenDepartment of Orthopedic Surgery, Mayo Clinic, Rochester, MN 55905, USA; Department of Biochemistry & Molecular Biology, Mayo Clinic, Rochester, MN 55905, USA. Electronic address: vanwijnen.andre@mayo.edu.
Hee-Jeong ImDepartment of Biochemistry, Rush University Medical Center, Chicago, IL 60612, USA; Department of Orthopedic Surgery, Rush University Medical Center, Chicago, IL 60612, USA; Department of Internal Medicine Section of Rheumatology, Rush University Medical Center, Chicago, IL 60612, USA; Department of Bioengineering, University of Illinois at Chicago, IL 60612, USA. Electronic address: Hee-Jeong_Sampen@rush.edu.
Rush University Medical Center · USChosun University · KRMayo Clinic · USPLA 306 Hospital · CN

Funding

Molecular Control of Bone FormationR01AR049069 · NIAMS · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI WESTENDORF, JENNIFER J · 2003 to 2021
$5.8M
The Mechanism through which TGF-Beta Maintains Chondrocytes in Proliferating StagR01AR054465 · NIAMS · UNIVERSITY OF ROCHESTER · PI CHEN, DI · 2007 to 2018
$2.7M
Pain Mechanisms of Knee Joint OsteoarthritisR01AR062136 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI CHEN, DI · 2012 to 2016
$1.7M
Beta-Catenin Signaling and Pathogenesis of OsteoarthritisR01AR055915 · NIAMS · UNIVERSITY OF ROCHESTER · PI CHEN, DI · 2009 to 2013
$1.7M
Pathological Role of bFGF in Human Adult Articular CartilageR01AR053220 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI SAMPEN, HEE-JEONG IM · 2006 to 2010
$1.6M
Allosteric Small Molecule Inhibitor Of Nerve Growth Factor Signaling in Low Back PainR21AR067935 · NIAMS · RUSH UNIVERSITY MEDICAL CENTER · PI CHEN, DI · 2015 to 2016
$375k
OSTEOARTHRITIS AND KNEE JOINT PAINI01BX002647 · VA · JESSE BROWN VA MEDICAL CENTER · PI SAMPEN, HEE-JEONG IM · 2015 to 2023
–
BLRD VA I01 BX002647NIAMS NIH HHS AR049069NIAMS NIH HHS AR053220NIAMS NIH HHS AR062136NIAMS NIH HHS R01 AR049069NIAMS NIH HHS R01 AR053220NIAMS NIH HHS R01 AR054465NIAMS NIH HHS R01 AR055915NIAMS NIH HHS R01 AR062136NIAMS NIH HHS R21 AR067935
6 · The paper itself

Abstract

Because miR-146a expression in articular chondrocytes is associated with osteoarthritis (OA), we assessed whether miR-146a is linked to cartilage degeneration in the spine. Monolayer cultures of nucleus pulposus (NP) cells from the intervertebral discs (IVD) of bovine tails were transfected with a miR-146a mimic. To provoke inflammatory responses and catabolic extracellular matrix (ECM) degradation, cells were co-treated with interleukin-1 (IL-1). Transfection of miR-146a decreases IL-1 induced mRNA levels of inflammatory genes and catabolic proteases in NP cells based on quantitative real-time reverse transcriptase PCR (qRT-PCR) analysis. Similarly, miR146a suppresses IL-1 induced protein levels of matrix metalloproteinases and aggrecanases as revealed by immunoblotting. Disc segments from wild type (WT) and miR-146a knockout (KO) mice were cultured ex vivo in the presence or absence of IL-1 for 3days. Histological and immuno-histochemical (IHC) analyses of disc organ cultures revealed that IL-1 mediates changes in proteoglycan (PG) content and in-situ levels of catabolic proteins (MMP-13 and ADAMTS-5) in the nucleus pulposus of the disc. However, these IL-1 effects are more pronounced in miR-146a KO discs compared to WT discs. For example, absence of miR-146a increases the percentage of MMP-13 and ADAMTS-5 positive cells after treatment with IL-1. Thus, miR-146a appears to protect against IL-1 induced IVD degeneration and inflammation. Stimulation of endogenous miR-146a expression or exogenous delivery of miRNA-146a are viable therapeutic strategies that may decelerate disc degeneration and regain a normal homeostatic balance in extracellular matrix production and turn-over.

Indexed as

Gene Expression RegulationADAM ProteinsADAMTS5 ProteinAnimalsCattleCells, CulturedExtracellular MatrixHomeostasisImmunohistochemistryInflammationInterleukin-1Intervertebral DiscIntervertebral Disc DegenerationIn Vitro TechniquesMatrix Metalloproteinase 13MiceADAM ProteinsADAMTS5 ProteinAdamts5 protein, mouseInterleukin-1Matrix Metalloproteinase 13MicroRNAsMirn146 microRNA, mouseMmp13 protein, mouseProteoglycansADAMTS-5IL-1Intervertebral disc degenerationmiR-146aMMP-13Nucleus pulposus

Identifiers

PMID25311550
PMCPMC4495656
OpenAlexW2023206100

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.