Evidence map›Paper›PMID 25793528›Full record

ArticlePloS one2015

Interferon-γ suppresses intestinal epithelial aquaporin-1 expression via Janus kinase and STAT3 activation.

Michael S Dicay, Christina L Hirota, Natalie J Ronaghan, Michael A Peplowski, Raza S Zaheer, Colin A Carati, Wallace K MacNaughton

Open 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. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

12 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
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  3. Targeting JAK/STAT signaling pathways in treatment of inflammatory bowel disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
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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

7 authors at 2 institutions in 2 countries.

Michael S DicayInflammation Research Network and Department of Physiology and Pharmacology, University of Calgary, Calgary, Canada.
Christina L HirotaInflammation Research Network and Department of Physiology and Pharmacology, University of Calgary, Calgary, Canada.
Natalie J RonaghanInflammation Research Network and Department of Physiology and Pharmacology, University of Calgary, Calgary, Canada.
Michael A PeplowskiInflammation Research Network and Department of Physiology and Pharmacology, University of Calgary, Calgary, Canada.
Raza S ZaheerInflammation Research Network and Department of Physiology and Pharmacology, University of Calgary, Calgary, Canada.
Colin A CaratiDepartment of Anatomy and Histology, Flinders University, Bedford Park, Australia.
Wallace K MacNaughtonInflammation Research Network and Department of Physiology and Pharmacology, University of Calgary, Calgary, Canada.
University of Calgary · CAFlinders University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory bowel diseases are associated with dysregulated electrolyte and water transport and resultant diarrhea. Aquaporins are transmembrane proteins that function as water channels in intestinal epithelial cells. We investigated the effect of the inflammatory cytokine, interferon-γ, which is a major player in inflammatory bowel diseases, on aquaporin-1 expression in a mouse colonic epithelial cell line, CMT93. CMT93 monolayers were exposed to 10 ng/mL interferon-γ and aquaporin-1 mRNA and protein expressions were measured by real-time PCR and western blot, respectively. In other experiments, CMT93 cells were pretreated with inhibitors or were transfected with siRNA to block the effects of Janus kinases, STATs 1 and 3, or interferon regulatory factor 2, prior to treatment with interferon-γ. Interferon-γ decreased aquaporin-1 expression in mouse intestinal epithelial cells in a manner that did not depend on the classical STAT1/JAK2/IRF-1 pathway, but rather, on an alternate Janus kinase (likely JAK1) as well as on STAT3. The pro-inflammatory cytokine, interferon-γ may contribute to diarrhea associated with intestinal inflammation in part through regulation of the epithelial aquaporin-1 water channel via a non-classical JAK/STAT receptor signalling pathway.

Indexed as

AnimalsAquaporin 1Cell LineEpithelial CellsGene Knockdown TechniquesInterferon-gammaInterferon Regulatory Factor-1Interferon Regulatory Factor-2IntestinesJanus KinasesMiceModels, BiologicalProtein Kinase InhibitorsRNA, MessengerSTAT1 Transcription FactorSTAT3 Transcription FactorAquaporin 1Interferon-gammaInterferon Regulatory Factor-1Interferon Regulatory Factor-2Irf2 protein, mouseJanus KinasesProtein Kinase InhibitorsRNA, MessengerSTAT1 Transcription FactorSTAT3 Transcription Factor

Identifiers

PMID25793528
PMCPMC4405000
OpenAlexW2064336913

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.