Evidence map›Paper›PMID 30589872›Full record

ArticlePloS one2018

A distinct epigenetic profile distinguishes stenotic from non-inflamed fibroblasts in the ileal mucosa of Crohn's disease patients.

Andrew Y F Li Yim, Jessica R de Bruyn, Nicolette W Duijvis, Catriona Sharp, Enrico Ferrero, Wouter J de Jonge, Manon E Wildenberg, Marcel M A M Mannens, Christianne J Buskens, Geert R D'Haens and 2 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. TET1 deficiency amplifies macrophage inflammatory signaling associated with Crohn's disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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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

12 authors at 2 institutions in 2 countries.

Andrew Y F Li YimGenome Diagnostics Laboratory, Department of Clinical Genetics, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.ORCID 0000-0002-0754-0953
Jessica R de BruynTytgat Institute for Liver and Intestinal Research, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Nicolette W DuijvisTytgat Institute for Liver and Intestinal Research, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.ORCID 0000-0002-3929-7978
Catriona SharpEpigenetics Discovery Performance Unit, GlaxoSmithKline, Stevenage, United Kingdom.
Enrico FerreroComputational Biology, Target Sciences, GlaxoSmithKline, Stevenage, United Kingdom.ORCID 0000-0002-8362-100X
Wouter J de JongeTytgat Institute for Liver and Intestinal Research, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Manon E WildenbergTytgat Institute for Liver and Intestinal Research, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Marcel M A M MannensGenome Diagnostics Laboratory, Department of Clinical Genetics, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Christianne J BuskensDepartment of Surgery, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Geert R D'HaensDepartment of Gastroenterology, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Peter HennemanGenome Diagnostics Laboratory, Department of Clinical Genetics, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Anje A Te VeldeTytgat Institute for Liver and Intestinal Research, Amsterdam UMC, University of Amsterdam, Amsterdam, the Netherlands.
Amsterdam University Medical Centers · NLGlaxoSmithKline (United Kingdom) · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe chronic remitting and relapsing intestinal inflammation characteristic of Crohn's disease frequently leads to fibrosis and subsequent stenosis of the inflamed region. Approximately a third of all Crohn's disease patients require resection at some stage in their disease course. As the pathogenesis of Crohn's disease associated fibrosis is largely unknown, a strong necessity exists to better understand the pathophysiology thereof.

methodsIn this study, we investigated changes of the DNA methylome and transcriptome of ileum-derived fibroblasts associated to the occurrence of Crohn's disease associated fibrosis. Eighteen samples were included in a DNA methylation array and twenty-one samples were used for RNA sequencing.

resultsMost differentially methylated regions and differentially expressed genes were observed when comparing stenotic with non-inflamed samples. By contrast, few differences were observed when comparing Crohn's disease with non-Crohn's disease, or inflamed with non-inflamed tissue. Integrative methylation and gene expression analyses revealed dysregulation of genes associated to the PRKACA and E2F1 network, which is involved in cell cycle progression, angiogenesis, epithelial to mesenchymal transition, and bile metabolism.

conclusionOur research provides evidence that the methylome and the transcriptome are systematically dysregulated in stenosis-associated fibroblasts.

Indexed as

Epigenesis, GeneticTranscriptomeAdultAgedComputational BiologyConstriction, PathologicCrohn DiseaseDNA MethylationGene Expression ProfilingGene Regulatory NetworksGenetic Predisposition to DiseaseHumansIntestinal MucosaMiddle AgedSeverity of Illness IndexYoung Adult

Identifiers

PMID30589872
PMCPMC6307755
OpenAlexW2907972922

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.