Evidence map›Paper›PMID 25586177›Full record

ArticleThe Journal of biological chemistry2015

Short term exposure of beta cells to low concentrations of interleukin-1β improves insulin secretion through focal adhesion and actin remodeling and regulation of gene expression.

Caroline Arous, Pedro G Ferreira, Emmanouil T Dermitzakis, Philippe A Halban

Erratum issuedOpen access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.0field-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

22 citing papers in PubMed, 32 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Caroline ArousFrom the Department of Genetic Medicine and Development, University Medical Centre, University of Geneva, 1211 Geneva 4, Switzerland Caroline.Arous@unige.ch.
Pedro G FerreiraFrom the Department of Genetic Medicine and Development, University Medical Centre, University of Geneva, 1211 Geneva 4, Switzerland.
Emmanouil T DermitzakisFrom the Department of Genetic Medicine and Development, University Medical Centre, University of Geneva, 1211 Geneva 4, Switzerland.
Philippe A HalbanFrom the Department of Genetic Medicine and Development, University Medical Centre, University of Geneva, 1211 Geneva 4, Switzerland.
University of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes involves defective insulin secretion with islet inflammation governed in part by IL-1β. Prolonged exposure of islets to high concentrations of IL-1β (>24 h, 20 ng/ml) impairs beta cell function and survival. Conversely, exposure to lower concentrations of IL-1β for >24 h improves these same parameters. The impact on insulin secretion of shorter exposure times to IL-1β and the underlying molecular mechanisms are poorly understood and were the focus of this study. Treatment of rat primary beta cells, as well as rat or human whole islets, with 0.1 ng/ml IL-1β for 2 h increased glucose-stimulated (but not basal) insulin secretion, whereas 20 ng/ml was without effect. Similar differential effects of IL-1β depending on concentration were observed after 15 min of KCl stimulation but were prevented by diazoxide. Studies on sorted rat beta cells indicated that the enhancement of stimulated secretion by 0.1 ng/ml IL-1β was mediated by the NF-κB pathway and c-JUN/JNK pathway acting in parallel to elicit focal adhesion remodeling and the phosphorylation of paxillin independently of upstream regulation by focal adhesion kinase. Because the beneficial effect of IL-1β was dependent in part upon transcription, gene expression was analyzed by RNAseq. There were 18 genes regulated uniquely by 0.1 but not 20 ng/ml IL-1β, which are mostly involved in transcription and apoptosis. These results indicate that 2 h of exposure of beta cells to a low but not a high concentration of IL-1β enhances glucose-stimulated insulin secretion through focal adhesion and actin remodeling, as well as modulation of gene expression.

Indexed as

ActinsAnimalsDiabetes Mellitus, Type 2Focal Adhesion Protein-Tyrosine KinasesFocal AdhesionsGene Expression RegulationGlucoseHumansInsulinInsulin-Secreting CellsInsulin SecretionInterleukin-1betaJNK Mitogen-Activated Protein KinasesMAP Kinase Signaling SystemPaxillinPrimary Cell CultureActinsFocal Adhesion Protein-Tyrosine KinasesGlucoseInsulinInterleukin-1betaJNK Mitogen-Activated Protein KinasesPaxillinActinActin RemodelingBeta cell (B-cell)c-JUN N-terminal kinase (JNK)ERK1/2Focal AdhesionsGene TranscriptionInsulin SecretionInterleukin-1β

Identifiers

PMID25586177
PMCPMC4358297
OpenAlexW1969874145

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.