Evidence map›Paper›PMID 23510983›Full record

ArticleIslets

Differential effects of interleukin-13 and interleukin-6 on Jak/STAT signaling and cell viability in pancreatic β-cells.

Mark A Russell, Angela C Cooper, Shalinee Dhayal, Noel G Morgan

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Islets. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
2.5field-weighted citation impact, top 11% 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, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  12. An Insulin-Inspired Supramolecular Hydrogel for Prevention of Type 1 Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2021
    Article
  13. Surfactant Protein-A Protects against IL-13-Induced Inflammation in Asthma.Journal of immunology (Baltimore, Md. : 1950) · 2020
    Article
  14. IL-4R is expressed on alpha and beta cells of human pancreata.Clinical immunology (Orlando, Fla.) · 2020
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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

4 authors at 2 institutions in 1 country.

Mark A RussellInstitute of Biomedical and Clinical Science, University of Exeter Medical School, Plymouth, Devon, UK.
Angela C Cooper
Shalinee Dhayal
Noel G Morgan
University of Exeter · GBUniversity of Plymouth · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pro-inflammatory cytokines are important mediators of β-cell demise in type 1 diabetes, and similar mechanisms are increasingly implicated in type 2 diabetes, where a state of chronic inflammation may persist. It is likely that the actions of anti-inflammatory cytokines are also altered in diabetes. Cytokines are released from immune cells, which may be recruited to the islets in diabetes, but they can also be produced by islet endocrine cells in response to environmental factors, including enteroviral infection. Since enteroviral infection of islet cells may influence the development of diabetes in humans, we examined the actions of two cytokines, IL-13 and IL-6, whose expression are reported to be altered in β-cells during enteroviral infection. Human and rodent islet cells were shown to express receptors for both IL-13 and IL-6, and treatment with either cytokine resulted in the rapid phosphorylation of STAT3 and STAT6. However, while β-cells were protected against a range of cytotoxic insults during exposure to IL-13, treatment with IL-6 enhanced cytotoxicity and western blotting revealed that IL-13 induced one specific isoform of phospho-STAT6 preferentially. Upon incubation with both cytokines together, the isoform of STAT6 that was upregulated by IL-13 alone was again induced, and the effects of IL-6 on β-cell viability were attenuated. Overall, the results suggest that induction of specific isoforms of STAT family transcription factors may underlie the cytoprotective actions of IL-13, and they imply that selective targeting of specific STAT-mediated signaling components could provide a means to ameliorate the loss of β-cell viability in diabetes.

Indexed as

Signal TransductionAnimalsCell LineCell SurvivalHumansInsulin-Secreting CellsInterleukin-13Interleukin-13 Receptor alpha1 SubunitInterleukin-6Islets of LangerhansJanus KinasesPhosphorylationProtein Processing, Post-TranslationalRatsReceptors, Interleukin-13Receptors, Interleukin-6IL13 protein, humanIL13RA1 protein, humanIL6 protein, humanIL6R protein, humanInterleukin-13Interleukin-13 Receptor alpha1 SubunitInterleukin-6Janus KinasesReceptors, Interleukin-13Receptors, Interleukin-6STAT3 protein, humanSTAT3 Transcription FactorSTAT6 protein, humanSTAT6 Transcription FactorSTAT Transcription Factorsinterleukin-13interleukin-6Janus kinasepancreatic β-cellsSTAT3STAT6

Identifiers

PMID23510983
PMCPMC4204019
OpenAlexW2048787600

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.