Evidence map›Paper›PMID 28737171›Full record

ArticleNature communications2017

BRG1-SWI/SNF-dependent regulation of the Wt1 transcriptional landscape mediates epicardial activity during heart development and disease.

Joaquim Miguel Vieira, Sara Howard, Cristina Villa Del Campo, Sveva Bollini, Karina N Dubé, Megan Masters, Damien N Barnette, Mala Rohling, Xin Sun, Laura E Hankins and 7 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
3.6field-weighted citation impact, top 6% 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

55 citing papers in PubMed, 89 citations in OpenAlex.

  1. Article
  2. Review
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  5. Article
  6. Review
  7. The molecular mechanisms of cardiac development and related diseases.Signal transduction and targeted therapy · 2024
    Review
  8. Review
  9. Epicardial EMT and cardiac repair: an update.Stem cell research & therapy · 2024
    Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. The regeneration-responsive elementFrontiers in molecular neuroscience · 2023
    Article
  20. 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

17 authors at 5 institutions in 2 countries.

Joaquim Miguel VieiraBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK.
Sara HowardMolecular Medicine Unit, UCL Institute of Child Health, London WC1N 1EH, UK.
Cristina Villa Del CampoBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK.
Sveva BolliniBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK.
Karina N DubéMolecular Medicine Unit, UCL Institute of Child Health, London WC1N 1EH, UK.
Megan MastersBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK.
Damien N BarnetteBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK.
Mala RohlingBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK.
Xin SunBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK.
Laura E HankinsBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK.
Daria GavriouchkinaWeatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Ruth WilliamsWeatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Daniel MetzgerInstitut de Génétique et de Biologie Moléculaire et Cellulaire, INSERM U964/CNRS UMR 7104/Université de Strasbourg, 67404 IllKirch Cedex, France.
Pierre ChambonInstitut de Génétique et de Biologie Moléculaire et Cellulaire, INSERM U964/CNRS UMR 7104/Université de Strasbourg, 67404 IllKirch Cedex, France.
Tatjana Sauka-SpenglerWeatherall Institute of Molecular Medicine, John Radcliffe Hospital, University of Oxford, Oxford OX3 9DS, UK.
Benjamin DaviesWellcome Trust Centre for Human Genetics, University of Oxford, Oxford OX3 7BN, UK.ORCID 0000-0003-3623-600X
Paul R RileyBurdon Sanderson Cardiac Science Centre, Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3PT, UK.
University of Oxford · GBJohn Radcliffe Hospital · GBCentre National de la Recherche Scientifique · FRUniversity College London · GBCentre for Human Genetics · GB

Funding

British Heart Foundation RG/08/003/25264British Heart Foundation RG/13/9/30269Medical Research Council G0902418
6 · The paper itself

Abstract

Epicardium-derived cells (EPDCs) contribute cardiovascular cell types during development and in adulthood respond to Thymosin β4 (Tβ4) and myocardial infarction (MI) by reactivating a fetal gene programme to promote neovascularization and cardiomyogenesis. The mechanism for epicardial gene (re-)activation remains elusive. Here we reveal that BRG1, the essential ATPase subunit of the SWI/SNF chromatin-remodelling complex, is required for expression of Wilms' tumour 1 (Wt1), fetal EPDC activation and subsequent differentiation into coronary smooth muscle, and restores Wt1 activity upon MI. BRG1 physically interacts with Tβ4 and is recruited by CCAAT/enhancer-binding protein β (C/EBPβ) to discrete regulatory elements in the Wt1 locus. BRG1-Tβ4 co-operative binding promotes optimal transcription of Wt1 as the master regulator of embryonic EPDCs. Moreover, chromatin immunoprecipitation-sequencing reveals BRG1 binding at further key loci suggesting SWI/SNF activity across the fetal epicardial gene programme. These findings reveal essential functions for chromatin-remodelling in the activation of EPDCs during cardiovascular development and repair.

Indexed as

Epigenesis, GeneticGenes, Wilms TumorAnimalsBase SequenceCCAAT-Enhancer-Binding Protein-betaChromatin Assembly and DisassemblyConserved SequenceDNA HelicasesGene Expression RegulationHeartHEK293 CellsHumansMiceMice, TransgenicMyocardial InfarctionNuclear ProteinsCCAAT-Enhancer-Binding Protein-betaDNA HelicasesNuclear ProteinsSMARCA4 protein, humanThymosinThymosin beta(4)Transcription Factors

Identifiers

PMID28737171
PMCPMC5527284
OpenAlexW2738998639

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.