Evidence map›Paper›PMID 26562662›Full record

ArticlePloS one2015

Interleukin (IL)-1β Is a Strong Inducer of IL-36γ Expression in Human Colonic Myofibroblasts.

Kenichiro Takahashi, Atsushi Nishida, Makoto Shioya, Hirotsugu Imaeda, Shigeki Bamba, Osamu Inatomi, Tomoharu Shimizu, Katsuyuki Kitoh, Akira Andoh

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

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.4field-weighted citation impact, top 12% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Review
  7. Article
  8. IL-36 in chronic inflammation and fibrosis - bridging the gap?The Journal of clinical investigation · 2021
    Review
  9. Review
  10. Article
  11. Article
  12. A cytokine network involving IL-36γ, IL-23, and IL-22 promotes antimicrobial defense and recovery from intestinal barrier damage.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  13. Article
  14. Article
  15. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Kenichiro TakahashiDepartment of Medicine, Shiga University of Medical Science, Seta-Tukinowa, Otsu 520-2192, Japan.
Atsushi NishidaDepartment of Medicine, Shiga University of Medical Science, Seta-Tukinowa, Otsu 520-2192, Japan.
Makoto ShioyaDepartment of Medicine, Shiga University of Medical Science, Seta-Tukinowa, Otsu 520-2192, Japan.
Hirotsugu ImaedaDepartment of Medicine, Shiga University of Medical Science, Seta-Tukinowa, Otsu 520-2192, Japan.
Shigeki BambaDepartment of Medicine, Shiga University of Medical Science, Seta-Tukinowa, Otsu 520-2192, Japan.
Osamu InatomiDepartment of Medicine, Shiga University of Medical Science, Seta-Tukinowa, Otsu 520-2192, Japan.
Tomoharu ShimizuDepartment of Surgery, Shiga University of Medical Science, Seta-Tukinowa, Otsu 520-2192, Japan.
Katsuyuki KitohDepartment of Medicine, Shiga University of Medical Science, Seta-Tukinowa, Otsu 520-2192, Japan.
Akira AndohDepartment of Medicine, Shiga University of Medical Science, Seta-Tukinowa, Otsu 520-2192, Japan.
Shiga University of Medical Science · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUNDS AND

aimsInterleukin (IL)-36 cytokines are members of the IL-1 cytokine family. In this study, we investigated the expression of IL-36γ in human colonic myofibroblasts to explore the molecular mechanisms underlying IL-36γ induction. MATERIALS AND

methodsIL-36 mRNA was analyzed by real-time PCR method. Secretion of IL-36γ protein was evaluated by Western blot and ELISA analyses. Molecular mechanism of IL-36γ induction was evaluated by siRNA analyses and immunofluorescence experiments.

resultsIL-36γ mRNA expression was scarcely detected in the cells without stimulation. IL-1β induced a marked increase of IL-36γ mRNA expression. TNF-α markedly enhanced IL-1β-induced IL-36γ mRNA expression. These responses were confirmed at the protein levels. The inhibitors for ERK1/2 (PD98059 and U0216) and a p38 MAPK (SB203580) significantly reduced the IL-1β-induced IL-36γ mRNA expression. In addition, the siRNAs specific for NF-κB p65 and AP-1 (c-Jun) significantly reduced the expression of IL-1β-induced IL-36γ mRNA.

conclusionsColonic myofibroblasts are cellular source of IL-36γ in the intestine. IL-36γ expression was induced by the combination of IL-1β and TNF-α via activation of MAPKs and transcription factors, NF-κB and AP-1.

Indexed as

Blotting, WesternButadienesCells, CulturedColonEnzyme-Linked Immunosorbent AssayExtracellular Signal-Regulated MAP KinasesFlavonoidsGene ExpressionHumansImidazolesInterleukin-1Interleukin-1betaMicroscopy, ConfocalMyofibroblastsNitrilesp38 Mitogen-Activated Protein Kinases2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-oneButadienesExtracellular Signal-Regulated MAP KinasesFlavonoidsIL36G protein, humanImidazolesInterleukin-1Interleukin-1betaNitrilesp38 Mitogen-Activated Protein KinasesPyridinesSB 203580Transcription Factor AP-1Transcription Factor RelATumor Necrosis Factor-alphaU 0126

Identifiers

PMID26562662
PMCPMC4643060
OpenAlexW2229266281

What OpenQuestion holds

Textmetadata
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.