Evidence map›Paper›PMID 29749927›Full record

ArticleeLife2018

The transcriptomic and epigenetic map of vascular quiescence in the continuous lung endothelium.

Katharina Schlereth, Dieter Weichenhan, Tobias Bauer, Tina Heumann, Evangelia Giannakouri, Daniel Lipka, Samira Jaeger, Matthias Schlesner, Patrick Aloy, Roland Eils and 2 more

Open access · goldAbstract readComparative Study
In one paragraph

Article in eLife, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.9field-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

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Expression status transition ofF1000Research · 2025
    Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. 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

12 authors at 3 institutions in 2 countries.

Katharina SchlerethEuropean Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.
Dieter WeichenhanDivision of Epigenomics and Cancer Risk Factors, German Cancer Research Center, Heidelberg, Germany.
Tobias BauerDivision of Theoretical Bioinformatics, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0002-4961-3639
Tina HeumannEuropean Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.
Evangelia GiannakouriEuropean Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.
Daniel LipkaDivision of Epigenomics and Cancer Risk Factors, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0001-5081-7869
Samira JaegerJoint IRB-BSC-CRG Program in Computational Biology, Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute for Science and Technology, Barcelona, Spain.
Matthias SchlesnerDivision of Theoretical Bioinformatics, German Cancer Research Center, Heidelberg, Germany.ORCID 0000-0002-5896-4086
Patrick AloyJoint IRB-BSC-CRG Program in Computational Biology, Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute for Science and Technology, Barcelona, Spain.
Roland EilsDivision of Theoretical Bioinformatics, German Cancer Research Center, Heidelberg, Germany.
Christoph Plass *Division of Epigenomics and Cancer Risk Factors, German Cancer Research Center, Heidelberg, Germany.
Hellmut G Augustin *European Center for Angioscience (ECAS), Medical Faculty Mannheim, Heidelberg University, Heidelberg, Germany.ORCID 0000-0002-7173-4242
German Cancer Research Center · DEInstitució Catalana de Recerca i Estudis Avançats · ESInstitute for Research in Biomedicine · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maintenance of a quiescent and organotypically-differentiated layer of blood vessel-lining endothelial cells (EC) is vital for human health. Yet, the molecular mechanisms of vascular quiescence remain largely elusive. Here we identify the genome-wide transcriptomic program controlling the acquisition of quiescence by comparing lung EC of infant and adult mice, revealing a prominent regulation of TGFß family members. These transcriptomic changes are distinctly accompanied by epigenetic modifications, measured at single CpG resolution. Gain of DNA methylation affects developmental pathways, including NOTCH signaling. Conversely, loss of DNA methylation preferentially occurs in intragenic clusters affecting intronic enhancer regions of genes involved in TGFβ family signaling. Functional experiments prototypically validated the strongly epigenetically regulated inhibitors of TGFβ family signaling SMAD6 and SMAD7 as regulators of EC quiescence. These data establish the transcriptional and epigenetic landscape of vascular quiescence that will serve as a foundation for further mechanistic studies of vascular homeostasis and disease-associated activation.

Indexed as

Epigenesis, GeneticGene Expression ProfilingAnimalsAnimals, NewbornBlood VesselsDNA MethylationEndothelial CellsEndotheliumLungMiceSmad6 ProteinSmad7 ProteinTranscription, GeneticTransforming Growth Factor betaSmad6 ProteinSmad6 protein, mouseSmad7 ProteinSmad7 protein, mouseTransforming Growth Factor betacomputational biologydevelopmental biologyDNA methylationendothelial epigenomeendothelial quiescenceendothelial trsanscriptomehumanmousestem cellssystems biologyTGFß

Identifiers

PMID29749927
PMCPMC5947988
OpenAlexW2802100792

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.