Evidence map›Paper›PMID 41167686›Full record

ArticleIn vivo (Athens, Greece)

Tripartite Motif-containing 22 Is Involved in TLR3-mediated Inflammatory Pathway in Rheumatoid Fibroblast-like Synoviocytes.

Kairo Wada, Hikaru Kristi Ishibashi, Yuzuru Nakamura, Tatsuro Saruga, Tadaatsu Imaizumi, Akira Kurose, Mayuki Tachizaki, Shogo Kawaguchi, Kazuhiko Seya, Kazuki Oishi and 3 more

Abstract read
In one paragraph

Article in In vivo (Athens, Greece). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Article
  2. Article
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

13 authors.

Kairo WadaDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan; h22gm126@hiroskai-u.ac.jp wadakai0909@outlook.jp.
Hikaru Kristi IshibashiDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Yuzuru NakamuraDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Tatsuro SarugaDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Tadaatsu ImaizumiDepartment of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Akira KuroseDepartment of Anatomic Pathology, Hirosaki University Graduate School of Medicine, Aomori, Japan.
Mayuki TachizakiDepartment of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Shogo KawaguchiDepartment of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Kazuhiko SeyaDepartment of Vascular and Inflammatory Medicine, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Kazuki OishiDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Eiji SasakiDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Kanichiro WadaDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.
Yasuyuki IshibashiDepartment of Orthopaedic Surgery, Hirosaki University Graduate School of Medicine, Hirosaki, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimRheumatoid arthritis (RA) is an autoimmune disease characterized by synovial inflammation and cartilage destruction. Tripartite motif-containing 22 (TRIM22) is involved in intracellular signal transduction, protein regulation, and innate immunity through E3 ubiquitin ligase activity. In this study, we examined the expression of TRIM22 and its potential role in synovial inflammation in RA. MATERIALS AND

methodsHuman rheumatoid fibroblast-like synoviocytes (RFLS) were cultured and treated with polyinosinic:polycytidylic acid (poly I:C), a toll-like receptor 3 (TLR3) ligand. Poly I:C was applied at different concentrations for different treatment durations. RNA interference was performed by pre-treating RFLS with either non-silencing control small interfering RNA (siRNA) or siRNA targeting

results

conclusionTreatment of cultured RFLS with a TLR3 agonist led to the upregulation of

Indexed as

Arthritis, RheumatoidInflammationRepressor ProteinsSynoviocytesToll-Like Receptor 3Cells, CulturedChemokine CCL5FibroblastsGene Expression RegulationHumansInterferon-betaMinor Histocompatibility AntigensNF-kappa BPoly I-CSignal TransductionSynovial MembraneChemokine CCL5Interferon-betaMinor Histocompatibility AntigensNF-kappa BPoly I-CRepressor ProteinsTLR3 protein, humanToll-Like Receptor 3TRIM22 protein, humanTripartite Motif ProteinsC-C motif chemokine ligand 5Rheumatoid arthritisrheumatoid fibroblast-like synoviocytestoll-like receptor 3tripartite motif-containing 22

Identifiers

PMID41167686
PMCPMC12588199

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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 Socratic graph.