Evidence map›Paper›PMID 21199896›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2011

IFN-γ attenuates hypoxia-inducible factor (HIF) activity in intestinal epithelial cells through transcriptional repression of HIF-1β.

Louise E Glover, Karina Irizarry, Melanie Scully, Eric L Campbell, Brittelle E Bowers, Carol M Aherne, Douglas J Kominsky, Christopher F MacManus, Sean P Colgan

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

16 citing papers in PubMed, 30 citations in OpenAlex.

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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

9 authors at 1 institution in 1 country.

Louise E GloverMucosal Inflammation Program, Department of Medicine, University of Colorado Denver, Aurora, CO 80045, USA.
Karina Irizarry
Melanie Scully
Eric L Campbell
Brittelle E Bowers
Carol M Aherne
Douglas J Kominsky
Christopher F MacManus
Sean P Colgan
University of Colorado Denver · US

Funding

ROLE OF EPITHELIA IN ISCHEMIA/REPERFUSION INJURYR01DK050189 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 2000 to 2024
$5.0M
Hypoxia, HIF, and Mucosal InflammationR37DK050189 · NIDDK · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 2010 to 2019
$4.1M
Neutrophils and Vascular Endothelial PermeabilityR01HL060569 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI COLGAN, SEAN P · 1999 to 2013
$3.5M
EPITHELIA AND ISCHEMIA/REPERFUSION INJURYR29DK050189 · NIDDK · BRIGHAM AND WOMEN'S HOSPITAL · PI COLGAN, SEAN P · 1995 to 1999
–
NHLBI NIH HHS HL60569NHLBI NIH HHS R01 HL060569NIDDK NIH HHS DK50189NIDDK NIH HHS R01 DK050189NIDDK NIH HHS R29 DK050189NIDDK NIH HHS R37 DK050189
6 · The paper itself

Abstract

Numerous studies have revealed that hypoxia and inflammation occur coincidentally in mucosal disorders, such as inflammatory bowel disease. During inflammation, epithelial-expressed hypoxia-inducible factor (HIF) serves an endogenously protective function. In this study, we sought to explore how mucosal immune responses influence HIF-dependent end points. Guided by a screen of relevant inflammatory mediators, we identified IFN-γ as a potent repressor of HIF-dependent transcription in human intestinal epithelial cells. Analysis of HIF levels revealed that HIF-1β, but not HIF-1α, is selectively repressed by IFN-γ in a JAK-dependent manner. Cloning and functional analysis of the HIF-1β promoter identified a prominent region for IFN-γ-dependent repression. Further studies revealed that colonic IFN-γ and HIF-1β levels were inversely correlated in a murine colitis model. Taken together, these studies demonstrated that intestinal epithelial HIF is attenuated by IFN-γ through transcriptional repression of HIF-1β. These observations are relevant to the pathophysiology of colitis (i.e., that loss of HIF signaling during active inflammation may exacerbate disease pathogenesis).

Indexed as

AnimalsAryl Hydrocarbon Receptor Nuclear TranslocatorCaco-2 CellsCell Line, TumorCells, CulturedCloning, MolecularColitisDextran SulfateDisease Models, AnimalFemaleHumansInflammation MediatorsInterferon-gammaIntestinal MucosaMiceMice, Inbred C57BLAryl Hydrocarbon Receptor Nuclear TranslocatorDextran SulfateInflammation MediatorsInterferon-gammaProcollagen-Proline DioxygenaseRepressor Proteins

Identifiers

PMID21199896
PMCPMC4040106
OpenAlexW1630611405

What OpenQuestion holds

Textmetadata
LicenceTDM
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.