Evidence map›Paper›PMID 21878622›Full record

ArticleThe Journal of biological chemistry2011

Interleukin-1beta induces increased transcriptional activation of the transforming growth factor-beta-activating integrin subunit beta8 through altering chromatin architecture.

Jennifer A Markovics, Jun Araya, Stephanie Cambier, Sangeeta Somanath, Stephanie Gline, David Jablons, Arthur Hill, Paul J Wolters, Stephen L Nishimura

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.0field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
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  6. Review
  7. Article
  8. Transcriptomic Profiling ofFrontiers in oncology · 2021
    Article
  9. Review
  10. Article
  11. Article
  12. Integrin Subunit beta 8 (ITGB8) Upregulation Is an Independent Predictor of Unfavorable Survival of High-Grade Serous Ovarian Carcinoma Patients.Medical science monitor : international medical journal of experimental and clinical research · 2018
    Article
  13. Article
  14. Article
  15. Article
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  17. Article
  18. Review
  19. Article
  20. Article
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 2 institutions in 2 countries.

Jennifer A MarkovicsDepartment Pathology, School of Medicine, University of California, San Francisco, California 94110, USA.
Jun Araya
Stephanie Cambier
Sangeeta Somanath
Stephanie Gline
David Jablons
Arthur Hill
Paul J Wolters
Stephen L Nishimura
University of California, San Francisco · USJikei University School of Medicine · JP

Funding

Integrin avB8 Inhibits Airway Epithelial Cell GrowthR01HL063993 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NISHIMURA, STEPHEN L · 2001 to 2011
$3.3M
Role of Squamous Metaplasia in Small Airways Disease in COPDR01HL090662 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI NISHIMURA, STEPHEN L · 2009 to 2010
$953k
NHLBI NIH HHS HL63993NHLBI NIH HHS R01 HL063993NHLBI NIH HHS R01 HL090662NINDS NIH HHS NS04415PHS HHS GU271119
6 · The paper itself

Abstract

The integrin αvβ8 is a cell surface receptor for the latent domain (LAP) of the multifunctional cytokine TGF-β. Through its association with LAP, TGF-β is maintained in a latent form that must be activated to function. Binding to the integrin αvβ8 with subsequent metalloproteolytic cleavage of LAP represents a major mechanism of TGF-β activation in vivo. Altered expression of the integrin β8 subunit (ITGB8) is found in human chronic obstructive pulmonary disease, cancers, and brain vascular malformations. We have previously shown that the proinflammatory cytokine interleukin-1β (IL-1β) increases ITGB8 expression on lung fibroblasts, which increases αvβ8-mediated TGF-β activation in fibrosis and pathologic inflammation. Here we report the mechanism of increased ITGB8 expression by IL-1β. Our data support a model where the chromatin architecture of the ITGB8 core promoter is altered by nucleosomal repositioning that enhances the interaction of an AP1 complex (containing c-Jun and ATF2). This repositioning is caused by the dissociation of HDAC2 with the ITGB8 core promoter, leading to increased histone H4 acetylation and a loosening of nucleosomal-DNA interactions allowing "opening" of the chromatin structure and increased association of c-Jun and ATF-2. These changes are mediated through NFκB- and p38-dependent pathways. Ultimately, these events culminate in increasing ITGB8 transcription, αvβ8 surface expression, and αvβ8-mediated TGFβ activation.

Indexed as

Chromatin Assembly and DisassemblyPromoter Regions, GeneticAcetylationActivating Transcription Factor 2ChromatinDNAHeLa CellsHistone Deacetylase 2HistonesHumansIntegrin alpha5Integrin beta ChainsInterleukin-1betaNF-kappa BNucleosomesProto-Oncogene Proteins c-junActivating Transcription Factor 2ATF2 protein, humanChromatinDNAHDAC2 protein, humanHistone Deacetylase 2HistonesIL1B protein, humanIntegrin alpha5Integrin beta ChainsInterleukin-1betaNF-kappa BNucleosomesProto-Oncogene Proteins c-junTransforming Growth Factor beta

Identifiers

PMID21878622
PMCPMC3196125
OpenAlexW2063764068

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.