Evidence map›Paper›PMID 31701670›Full record

ArticleJournal of cellular and molecular medicine2020

The pro-inflammatory effect of NR4A3 in osteoarthritis.

Chiyuan Ma, Lingyun Wu, Lu Song, Yuzhe He, Safwat Adel Abdo Moqbel, Shigui Yan, Kunkun Sheng, Haobo Wu, Jisheng Ran, Lidong Wu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.5field-weighted citation impact, top 4% 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

29 citing papers in PubMed, 55 citations in OpenAlex.

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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

10 authors at 2 institutions in 1 country.

Chiyuan MaDepartment of Orthopedics Surgery, The 2nd Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Lingyun WuDepartment of Radiation Oncology, The 1st Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Lu SongDepartment of Stomatology, Huaihe Hospital of Henan University, Kaifeng, China.
Yuzhe HeDepartment of Orthopedics Surgery, The 2nd Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Safwat Adel Abdo MoqbelDepartment of Orthopedics Surgery, The 2nd Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Shigui YanDepartment of Orthopedics Surgery, The 2nd Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Kunkun ShengDepartment of Orthopedics Surgery, The 2nd Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Haobo WuDepartment of Orthopedics Surgery, The 2nd Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Jisheng RanDepartment of Orthopedics Surgery, The 2nd Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.
Lidong WuDepartment of Orthopedics Surgery, The 2nd Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China.ORCID 0000-0002-2561-6069
Second Affiliated Hospital of Zhejiang University · CNHenan University Huaihe Hospital and Huaihe Clinical Institute · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

NR4A3 is a member of nuclear receptor subfamily 4, which is an important regulator of cellular function and inflammation. In this study, high expression of NR4A3 in human osteoarthritis (OA) cartilage was firstly observed. To explore the relationship between NR4A3 and OA, we used a lentivirus overexpression system to simulate its high expression and study its role in OA. Additionally, siRNA-mediated knockdown of NR4A3 was used to confirm the findings of overexpression experiments. The results showed the stimulatory effect of IL-1β on cartilage matrix-degrading enzyme expression such as MMP-3, 9, INOS and COX-2 was enhanced in NR4A3-overexpressed chondrocytes and decreased in NR4A3-knockdown chondrocytes at both mRNA and protein levels, while IL-1β-induced chondrocyte-specific gene (collagen 2 and SOX-9) degradation was only regulated by NR4A3 at protein level. Furthermore, overexpression of NR4A3 would also enhance EBSS-induced chondrocytes apoptosis, while knockdown of NR4A3 decreased apoptotic level after EBSS treatment. A pathway study indicated that IL-1β-induced NF-κB activation was enhanced by NR4A3 overexpression and reduced by NR4A3 knockdown. We suggest that NR4A3 plays a pro-inflammatory role in the development of OA, and we also speculate that NR4A3 mainly regulates cartilage matrix-degrading gene expression under inflammatory conditions via the NF-κB pathway.

Indexed as

Gene Expression RegulationAnimalsApoptosisCase-Control StudiesCells, CulturedChondrocytesDNA-Binding ProteinsFemaleHumansInflammationMaleOsteoarthritisRatsRats, Sprague-DawleyReceptors, SteroidReceptors, Thyroid HormoneDNA-Binding ProteinsNR4A3 protein, humanReceptors, SteroidReceptors, Thyroid HormonechondrocyteNF-κBNR4A3osteoarthritis

Identifiers

PMID31701670
PMCPMC6933326
OpenAlexW2989075544

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.