Evidence map›Paper›PMID 22911824›Full record

ArticlePloS one2012

Fra-1/AP-1 transcription factor negatively regulates pulmonary fibrosis in vivo.

Subbiah Rajasekaran, Michelle Vaz, Sekhar P Reddy

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

23 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
  2. Review
  3. Epigenetic Modifications in the Pathogenesis of Systemic Sclerosis.International journal of general medicine · 2022
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Identifying collagen VI as a target of fibrotic diseases regulated by CREBBP/EP300.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Matrix metalloproteinases as therapeutic targets for idiopathic pulmonary fibrosis.American journal of respiratory cell and molecular biology · 2015
    Review
  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

3 authors at 1 institution in 1 country.

Subbiah RajasekaranDepartment of Pediatrics, University of Illinois at Chicago, Chicago, Illinois, United States of America.
Michelle Vaz
Sekhar P Reddy
Johns Hopkins University · US

Funding

Human NRF2 Promoter Functional Polymorphisms and Acute Lung InjuryR01HL066109 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI REDDY, SEKHAR P. · 2001 to 2012
$3.5M
The Role and Biology of Fra-1 in Lung Injury and RepairR01ES011863 · NIEHS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI REDDY, SEKHAR P. · 2002 to 2013
$3.4M
Targeting Fra-1 in Toxicant-Induced Lung Tumor Initiation & DevelopmentR21ES018998 · NIEHS · UNIVERSITY OF ILLINOIS AT CHICAGO · PI REDDY, SEKHAR P. · 2011 to 2012
$430k
NHLBI NIH HHS R01 HL066109NHLBI NIH HHS R01 HL66109NIEHS NIH HHS R01 ES011863NIEHS NIH HHS R01 ES11863NIEHS NIH HHS R21 ES018998NIEHS NIH HHS R21 ES18998
6 · The paper itself

Abstract

The Fra-1/AP-1 transcription factor plays a key role in tumor epithelial cell progression; however, its role in pathogenic lung fibrosis remains unclear. In the present study, using a genetic approach (Fra-1 deficient mice), we have demonstrated a novel regulatory (protective) role for Fra-1 in lung fibrosis. We found greater levels of progressive interstitial fibrosis, characterized by increased levels of inflammation, collagen accumulation, and profibrotic and fibrotic gene expression in the lungs of Fra-1(Δ/Δ) mice than in those of Fra-1(+/+) mice following bleomycin treatment. Fra-1 knockdown in human lung epithelial cells caused the upregulation of mesenchymal marker N-cadherin, concomitant with a downregulation of the epithelial phenotype marker E-cadherin, under basal conditions and in response to bleomycin and TGF-β1. Furthermore, Fra-1 knockdown caused an enhanced expression of type 1 collagen and the downregulation of collagenase (MMP-1 and MMP-13) gene expression in human lung epithelial cells. Collectively, our findings demonstrate that Fra-1 mediates anti-fibrotic effects in the lung through the modulation of proinflammatory, profibrotic and fibrotic gene expression, and suggests that the Fra-1 transcription factor may be a potential target for pulmonary fibrosis, a progressive disorder with poor prognosis and treatment.

Indexed as

AnimalsBleomycinCytokinesEpithelial CellsFos-Related Antigen 1Gene DeletionGene Expression RegulationGene Knockdown TechniquesHumansInflammation MediatorsLungMatrix MetalloproteinasesMiceMice, Inbred C57BLPneumoniaProto-Oncogene Proteins c-fosBleomycinCytokinesFos-Related Antigen 1Inflammation MediatorsMatrix MetalloproteinasesProto-Oncogene Proteins c-fosTissue Inhibitor of MetalloproteinasesTranscription Factor AP-1Transforming Growth Factor beta1

Identifiers

PMID22911824
PMCPMC3404039
OpenAlexW1988933960

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.