Evidence map›Paper›PMID 16682432›Full record

ArticleGut2006

STAT3 activation via interleukin 6 trans-signalling contributes to ileitis in SAMP1/Yit mice.

K Mitsuyama, S Matsumoto, S Rose-John, A Suzuki, T Hara, N Tomiyasu, K Handa, O Tsuruta, H Funabashi, J Scheller and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in Gut, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

49 citing papers in PubMed, 120 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Heliyon · 2022
    Article
  7. Article
  8. Review
  9. Review
  10. Endosomes as Signaling Platforms for IL-6 Family Cytokine Receptors.Frontiers in cell and developmental biology · 2021
    Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Interleukin-6 Family Cytokines.Cold Spring Harbor perspectives in biology · 2018
    Review
  17. Role of ADAM10 in intestinal crypt homeostasis and tumorigenesis.Biochimica et biophysica acta. Molecular cell research · 2017
    Review
  18. Review
  19. Nicotine protects against DSS colitis through regulating microRNA-124 and STAT3.Journal of molecular medicine (Berlin, Germany) · 2017
    Article
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 2 countries.

K MitsuyamaSecond Department of Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume, Fukuoka 830-0011, Japan. ibd@med.kurume-u.ac.jp
S Matsumoto
S Rose-John
A Suzuki
T Hara
N Tomiyasu
K Handa
O Tsuruta
H Funabashi
J Scheller
A Toyonaga
M Sata
Kurume University · JPKiel University · DEYakult Central Institute · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND AND

aimsSAMP1/Yit mice spontaneously develops intestinal inflammation. Previously, we demonstrated that the signal transducer and activator of transcription (STAT)-3/suppressor of cytokine signalling (SOCS)-3 pathway is pivotal in human inflammatory bowel disease. In our studies in SAMP1/Yit mice, the aim was to investigate whether STAT3 activation contributes to ileitis and to examine the therapeutic effects of this signal blockade.

methodsIntestinal expression of phospho-STAT3 in SAMP1/Yit mice and control AKR/J mice was examined by western blotting and immunohistochemistry. SOCS3 and interleukin 6 (IL-6) mRNA were determined by northern blotting and reverse transcription-polymerase chain reaction, respectively. We also examined the effects of intravenously injected hyper-IL-6, an IL-6/soluble IL-6 receptor fusion protein, and of soluble gp130-Fc, a specific inhibitor of soluble IL-6 receptor signalling, on STAT3 phosphorylation and disease severity in SAMP1/Yit mice.

resultsPhospho-STAT3 was expressed strongly during the disease course in SAMP1/Yit mice but only transiently in AKR/J mice. Phospho-STAT3 was localised to epithelial and mononuclear cells in the diseased intestine of SAMP1/Yit mice. SOCS3 as well as IL-6 mRNAs were expressed in affected intestine. Administration of hyper-IL-6 caused disease exacerbation and enhancement of STAT3 phosphorylation. In contrast, soluble gp130-Fc administration ameliorated the disease and suppressed STAT3 phosphorylation.

conclusionSTAT3 signalling is critical in the development of intestinal inflammation in SAMP1/Yit mice. Blockade of this signalling pathway by soluble gp130-Fc may have therapeutic effects in inflammatory bowel disease.

Indexed as

Disease Models, AnimalAnimalsDown-RegulationGene ExpressionGlycoproteinsIleitisIleumInflammatory Bowel DiseasesInterleukin-6MiceMice, Inbred StrainsPhosphorylationRNA, MessengerSignal TransductionSTAT3 Transcription FactorSuppressor of Cytokine Signaling Proteinsglycoprotein 130, humanGlycoproteinsInterleukin-6RNA, MessengerStat3 protein, mouseSTAT3 Transcription FactorSuppressor of Cytokine Signaling Proteins

Identifiers

PMID16682432
PMCPMC1860050
OpenAlexW2157233685

What OpenQuestion holds

Textmetadata
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.