Evidence map›Paper›PMID 26659307›Full record

ArticlePloS one2015

Examination of a Viral Infection Mimetic Model in Human iPS Cell-Derived Insulin-Producing Cells and the Anti-Apoptotic Effect of GLP-1 Analogue.

Megu Yamaguchi Baden, Kenji Fukui, Yoshiya Hosokawa, Hiromi Iwahashi, Akihisa Imagawa, Iichiro Shimomura

Open access · goldAbstract read
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. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

5 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
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  4. Review
  5. Review
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

6 authors at 1 institution in 1 country.

Megu Yamaguchi BadenDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.
Kenji FukuiDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.
Yoshiya HosokawaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.
Hiromi IwahashiDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.
Akihisa ImagawaDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.
Iichiro ShimomuraDepartment of Metabolic Medicine, Graduate School of Medicine, Osaka University, Suita, Japan.
Osaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsViral infection is associated with pancreatic beta cell destruction in fulminant type 1 diabetes mellitus. The aim of this study was to investigate the acceleration and protective mechanisms of beta cell destruction by establishing a model of viral infection in pancreatic beta cells.

methodsPolyinosinic:polycytidylic acid was transfected into MIN6 cells and insulin-producing cells differentiated from human induced pluripotent stem cells via small molecule applications. Gene expression was analyzed by real-time PCR, and apoptosis was evaluated by caspase-3 activity and TUNEL staining. The anti-apoptotic effect of Exendin-4 was also evaluated.

resultsPolyinosinic:polycytidylic acid transfection led to elevated expression of the genes encoding IFNα, IFNβ, CXCL10, Fas, viral receptors, and IFN-inducible antiviral effectors in MIN6 cells. Exendin-4 treatment suppressed the elevated gene expression levels and reduced polyinosinic:polycytidylic acid-induced apoptosis both in MIN6 cells and in insulin-producing cells from human induced pluripotent stem cells. Glucagon-like peptide-1 receptor, protein kinase A, and phosphatidylinositol-3 kinase inhibitors counteracted the anti-apoptotic effect of Exendin-4.

conclusionsPolyinosinic:polycytidylic acid transfection can mimic viral infection, and Exendin-4 exerted an anti-apoptotic effect both in MIN6 and insulin-producing cells from human induced pluripotent stem cells.

Indexed as

Models, BiologicalAntiviral AgentsApoptosisCell DifferentiationCells, CulturedChemokine CXCL10Cyclic AMP-Dependent Protein KinasesEnzyme InhibitorsExenatidefas ReceptorGene Expression RegulationGlucagon-Like Peptide-1 ReceptorHumansHypoglycemic AgentsInduced Pluripotent Stem CellsInsulin-Secreting CellsAntiviral AgentsChemokine CXCL10CXCL10 protein, humanCyclic AMP-Dependent Protein KinasesEnzyme InhibitorsExenatideFAS protein, humanfas ReceptorGlucagon-Like Peptide-1 ReceptorHypoglycemic AgentsInterferon-alphaInterferon-betaInterferon InducersPeptidesPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsPoly I-CReceptors, VirusVenoms

Identifiers

PMID26659307
PMCPMC4676675
OpenAlexW2191317660

What OpenQuestion holds

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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.