Evidence map›Paper›PMID 36114544›Full record

ArticleArthritis research & therapy2022

Role of DNA dioxygenase Ten-Eleven translocation 3 (TET3) in rheumatoid arthritis progression.

Akio Kawabe, Kaoru Yamagata, Shigeaki Kato, Kazuhisa Nakano, Kei Sakata, Yu-Ichi Tsukada, Koichiro Ohmura, Shingo Nakayamada, Yoshiya Tanaka

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arthritis research & therapy, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.8field-weighted citation impact, top 31% 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

7 citing papers in PubMed, 10 citations in OpenAlex.

  1. Review
  2. Mechanisms of mitral valve development and disease.Frontiers in cardiovascular medicine · 2026
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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 5 institutions in 1 country.

Akio KawabeThe First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahatanishi, Kitakyushu, 807-8555, Japan.
Kaoru YamagataThe First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahatanishi, Kitakyushu, 807-8555, Japan.
Shigeaki KatoHealth Sciences Research Center, Iryo Sosei University, 5-5-1 Chuodai-iino, Iwaki, Fukushima, 970-8551, Japan.
Kazuhisa NakanoThe First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahatanishi, Kitakyushu, 807-8555, Japan.
Kei SakataThe First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahatanishi, Kitakyushu, 807-8555, Japan.
Yu-Ichi TsukadaAdvanced Biological Information Research Division, AMORI Frontier Research Center, Kyushu University, 744 Motooka, Nishi, Fukuoka, 819-0395, Japan.
Koichiro OhmuraDepartment of Rheumatology and Clinical Immunology, Graduate School of Medicine, Kyoto University, 54 Shogoin-kawara, Sakyo, Kyoto, 606-8507, Japan.
Shingo NakayamadaThe First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahatanishi, Kitakyushu, 807-8555, Japan.
Yoshiya TanakaThe First Department of Internal Medicine, School of Medicine, University of Occupational and Environmental Health, Japan, 1-1 Iseigaoka, Yahatanishi, Kitakyushu, 807-8555, Japan. tanaka@med.uoeh-u.ac.jp.ORCID 0000-0002-0807-7139
University of Occupational and Environmental Health Japan · JPJyoban Hospital of Tokiwa Foundation · JPKyoto University · JPKyushu University · JPMitsubishi Chemical (Japan) · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundRheumatoid arthritis (RA) patients present with abnormal methylation patterns in their fibroblast-like synoviocytes (FLS). Given that DNA demethylation is critical for producing DNA methylation patterns, we hypothesized that DNA demethylation may facilitate RA progression. Therefore, we designed this study to examine the role of DNA dioxygenase family, Ten-Eleven translocation (TET1/2/3), in the pathological process of RA.

methodsSynovial tissues and FLS were obtained from patients with RA and Osteoarthritis. K/BxN serum-induced arthritis was induced in Wild-type (WT) and TET3 heterozygous-deficient (TET3

resultsWe found that both TET3 and 5-hydroxymethylcytosine (5hmC) were upregulated in synovitis tissues from RA patients and confirmed this upregulation in the cultured FLS derived from synovitis tissues. Tumor necrosis factor α (TNFα) upregulated TET3 and 5hmC levels in cultured FLS, and the stimulated FLS exhibited high cell mobility with increased transcription of cellular migration-related factors such as C-X-C motif chemokine ligand 8 (CXCL8) and C-C motif chemokine ligand 2 (CCL2) in a TET3-dependent manner. In addition, TET3 haploinsufficiency lowered RA progression in a mouse model of serum-induced arthritis.

conclusionsBased on these findings, we can assume that TET3-mediated DNA demethylation acts as an epigenetic regulator of RA progression.

Indexed as

Arthritis, RheumatoidSynovitisAnimalsChemokinesDioxygenasesDNALigandsMiceMice, Inbred C57BLTumor Necrosis Factor-alphaChemokinesDioxygenasesDNALigandsTet3 protein, mouseTumor Necrosis Factor-alphaFibroblast-like synoviocytesRheumatoid arthritisTen-Eleven translocation 3Tumor necrosis factor α

Identifiers

PMID36114544
PMCPMC9479255
OpenAlexW4296164581

What OpenQuestion holds

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LicenceCC BY
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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.