Evidence map›Paper›PMID 31343104›Full record

ArticleCell proliferation2019

miR-640 aggravates intervertebral disc degeneration via NF-κB and WNT signalling pathway.

Wengang Dong, Jun Liu, Yang Lv, Fei Wang, Tao Liu, Siguo Sun, Bo Liao, Zhen Shu, Jixian Qian

Open access · goldAbstract read
In one paragraph

Article in Cell proliferation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
6.6field-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

59 citing papers in PubMed, 82 citations in OpenAlex.

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  12. AEuropean journal of medical research · 2024
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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

9 authors at 4 institutions in 2 countries.

Wengang DongDepartment of Orthopaedics, The Second Affiliated Hospital of Air Force Medical University, Xi'an, China.
Jun LiuLaboratory of Molecular Biology, Disease Control and Prevention Center of PLA's Southern Theatre Command, Guangzhou, China.
Yang LvDepartment of Orthopaedics, General Hospital of Lanzhou Military Command, Lanzhou, China.
Fei WangDepartment of Orthopaedics, General Hospital of Lanzhou Military Command, Lanzhou, China.
Tao LiuDepartment of Orthopaedics, The Second Affiliated Hospital of Air Force Medical University, Xi'an, China.
Siguo SunDepartment of Orthopaedics, The Second Affiliated Hospital of Air Force Medical University, Xi'an, China.
Bo LiaoDepartment of Orthopaedics, The Second Affiliated Hospital of Air Force Medical University, Xi'an, China.
Zhen ShuDepartment of Radiation Oncology, Winship Cancer Institute, Emory University School of Medicine, Atlanta, GA, USA.ORCID https://orcid.org/0000-0002-4088-6438
Jixian QianDepartment of Orthopaedics, The Second Affiliated Hospital of Air Force Medical University, Xi'an, China.
Air Force Medical University · CNLanzhou Army General Hospital · CNEmory University · USThird Affiliated Hospital of Southern Medical University · CN

Funding

National Natural Science Foundation of China 31601096National Natural Science Foundation of China 81871818Science and Technology Research and Development Projects of Shaanxi Province 2016SF-140
6 · The paper itself

Abstract

objectivesLow back pain becomes a common orthopaedic disease today. It is mainly induced by the degeneration of the intervertebral disc. In this study, we tried to reveal the pathogenesis of the degeneration and the relative therapeutic strategy, which are still elusive. MATERIALS AND

methodsWe collected 15 degenerative intervertebral tissues and five healthy donors. Nucleus pulposus and annulus fibrosus cells were subcultured. miR-640 expression was determined by qPCR. Computer analysis and luciferase reporter assay were used to confirm miR-640 target genes. Immunohistochemical and immunocytochemical staining was used to trace the proinflammatory cytokines and key transductor of signalling pathways. We also used β-galactosidase staining, flow cytometry, and cell viability assay to monitor the degenerative index.

resultsmiR-640 overexpressed in patients derived degenerative nucleus pulposus tissues and cells. The inflammatory environment promoted miR-640 expression via NF-κB signalling pathway. In addition, miR-640 targeted to LRP1 and enhances NF-κB signal activity, which built a positive feedback loop. miR-640 inhibited the expression of β-catenin and EP300, therefore, restrained WNT signal and induced the degeneration in nucleus pulposus cells. miR-640 inhibitor treatment exhibited the effects of anti-inflammation, reverse WNT signalling pathway exhaustion, and remission of degenerative characteristics in vitro.

conclusionsmiR-640 plays an important role in the degeneration of intervertebral disc and the relative inflammatory microenvironment. It is a promising potential therapeutic target for the low back pain biotherapy.

Indexed as

Signal TransductionAdolescentAdultAnnulus FibrosusAntagomirsbeta CateninCase-Control StudiesCells, CulturedE1A-Associated p300 ProteinHumansInterleukin-1betaIntervertebral Disc DegenerationLow Density Lipoprotein Receptor-Related Protein-1MicroRNAsMiddle AgedNF-kappa BAntagomirsbeta CateninE1A-Associated p300 ProteinEP300 protein, humanInterleukin-1betaLow Density Lipoprotein Receptor-Related Protein-1LRP1 protein, humanMicroRNAsMIRN640 microRNA, humanNF-kappa BRELA protein, humanTranscription Factor RelAWnt Proteinsinflammationintervertebral disc degenerationmicroRNAnucleus pulposusWNT signalling pathway

Identifiers

PMID31343104
PMCPMC6797513
OpenAlexW2963715560

What OpenQuestion holds

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LicenceCC BY
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.