Evidence map›Paper›PMID 23635716›Full record

ArticleInflammatory bowel diseases2013

Cytokine-induced chromatin modifications of the type I collagen alpha 2 gene during intestinal endothelial-to-mesenchymal transition.

Tammy Sadler, Melania Scarpa, Florian Rieder, Gail West, Eleni Stylianou

Open access · bronzeAbstract read
In one paragraph

Article in Inflammatory bowel diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.6field-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

20 citing papers in PubMed, 40 citations in OpenAlex.

  1. Review
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  8. Genes · 2023
    Article
  9. Review
  10. Review
  11. Review
  12. Review
  13. Review
  14. Genetic and epigenetic regulation of intestinal fibrosis.United European gastroenterology journal · 2016
    Review
  15. TGF-β receptor 1 inhibition prevents stenosis of tissue-engineered vascular grafts by reducing host mononuclear phagocyte activation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016
    Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Epigenetics: the fine-tuner in inflammatory bowel disease?Current opinion in gastroenterology · 2013
    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

5 authors at 1 institution in 1 country.

Tammy SadlerDepartment of Pathobiology, Lerner Research Institute, Cleveland, Ohio, USA.
Melania Scarpa
Florian Rieder
Gail West
Eleni Stylianou
Cleveland Clinic Lerner College of Medicine · US

Funding

Combined Training Program in Digestive Disease SciencesT32DK083251 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI COMINELLI, FABIO, FIOCCHI, CLAUDIO · 2010 to 2025
$3.6M
Cell interactions in the inflammed intestinal mucosaR01DK050984 · NIDDK · CLEVELAND CLINIC LERNER COM-CWRU · PI FIOCCHI, CLAUDIO · 1995 to 2014
$3.1M
NIDDK NIH HHS DK50984NIDDK NIH HHS R01 DK050984NIDDK NIH HHS T32 DK083251
6 · The paper itself

Abstract

backgroundFibrosis of the intestine is currently an irreversible complication of inflammatory bowel disease; yet, little is understood of the underlying pathogenesis and antifibrotic strategies remain elusive. To develop effective therapies, knowledge of the mechanism of transcription and excessive deposition of type I collagen, a hallmark of fibrosis, is needed. We have shown previously that endothelial-to-mesenchymal transition (EndoMT) contributes to the pool of intestinal fibrotic cells and that a cytokine cocktail (interleukin 1-β, tumor necrosis factor α, and transforming growth factor β) induces collagen I alpha 2 (COL1A2) mRNA and protein.

methodsChromatin immunoprecipitation assays on pure cultures of human intestinal mucosal endothelial cells undergoing EndoMT were performed with antibodies to specific histone modifications and RNA polymerase II. Reverse transcriptase-PCR was used to quantify the levels of Col1A2 and endothelial-specific von Willebrand factor (vWF) mRNA.

resultsWe showed that cytokines induce selective chromatin modifications (histone 4 hyperacetylation, and hypermethylation of histone 3) and phosphorylated RNA polymerase II at the COL1A2 promoter. Hypoacetylated and hypomethylated histone 3 was detected on the repressed vWF gene. Prolonged exposure to cytokines (16 days) retained hyperacetylation of select lysines in H4 on the COL1A2 promoter. Removal of cytokines after 16 days and continued culture for 10 days showed persistent hyperacetylation at lysine 16 in histone H4.

conclusionsThis is the first study to show that COL1A2 gene expression is associated with cytokine-induced, temporally ordered, and persistent chromatin modifications and suggests that these are important determinants of gene expression in EndoMT and intestinal fibrosis.

Indexed as

Blotting, WesternCells, CulturedChromatinChromatin ImmunoprecipitationCollagen Type IDNA MethylationEndothelium, VascularFibrosisHistonesHumansInterleukin-1betaIntestinal MucosaLysineMesodermPromoter Regions, GeneticReal-Time Polymerase Chain ReactionChromatinCollagen Type IHistonesInterleukin-1betaLysineRNA, MessengerRNA Polymerase IITransforming Growth Factor beta1Tumor Necrosis Factor-alpha

Identifiers

PMID23635716
PMCPMC3684204
OpenAlexW2054966459

What OpenQuestion holds

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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.