Evidence map›Paper›PMID 31369967›Full record

ArticleCytokine2019

Activin A-mediated epithelial de-differentiation contributes to injury repair in an in vitro gastrointestinal reflux model.

Cedric Roudebush, Alma Catala-Valentin, Thomas Andl, Gregoire F Le Bras, Claudia D Andl

Open access · greenAbstract read
In one paragraph

Article in Cytokine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

11 citing papers in PubMed, 14 citations in OpenAlex.

  1. Trial
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  7. Mechanisms and pathophysiology of Barrett oesophagus.Nature reviews. Gastroenterology & hepatology · 2022
    Review
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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

5 authors at 1 institution in 1 country.

Cedric RoudebushBurnett School of Biomedical Sciences, University of Central Florida, 4110 Libra Dr., BMS, Building 20, rm 223, Orlando, FL 32816, United States.
Alma Catala-ValentinBurnett School of Biomedical Sciences, University of Central Florida, 4110 Libra Dr., BMS, Building 20, rm 223, Orlando, FL 32816, United States.
Thomas AndlBurnett School of Biomedical Sciences, University of Central Florida, 4110 Libra Dr., BMS, Building 20, rm 223, Orlando, FL 32816, United States.
Gregoire F Le BrasBurnett School of Biomedical Sciences, University of Central Florida, 4110 Libra Dr., BMS, Building 20, rm 223, Orlando, FL 32816, United States.
Claudia D AndlBurnett School of Biomedical Sciences, University of Central Florida, 4110 Libra Dr., BMS, Building 20, rm 223, Orlando, FL 32816, United States. Electronic address: Claudia.andl@ucf.edu.
University of Central Florida · US

Funding

The role of Activin A signaling in esophageal cell invasionR01DK094900 · NIDDK · VANDERBILT UNIVERSITY · PI ANDL, CLAUDIA D · 2012 to 2016
$1.6M
NIDDK NIH HHS R01 DK094900
6 · The paper itself

Abstract

Reflux esophagitis is a result of esophageal exposure to acid and bile during episodes of gastroesophageal reflux. Aside from chemical injury to the esophageal epithelium, it has been shown that acid and bile induce cytokine-mediated injury by stimulating the release of pro-inflammatory cytokines. During the repair and healing process following reflux injury, the squamous esophageal cells are replaced with a columnar epithelium causing Barrett's metaplasia, which predisposes patients to esophageal adenocarcinoma. We identified a novel player in gastroesophageal reflux injury, the TGFβ family member Activin A (ActA), which is a known regulator of inflammation and tissue repair. In this study, we show that in response to bile salt and acidified media (pH 4) exposure, emulating the milieu to which the distal esophagus is exposed during gastroesophageal reflux, long-term treated, tolerant esophageal keratinocytes exhibit increased ActA secretion and a pro-inflammatory cytokine signature. Furthermore, we noted increased motility and expression of the stem cell markers SOX9, LGR5 and DCLK1 supporting the notion that repair mechanisms were activated in the bile salt/acid-tolerant keratinocytes. Additionally, these experiments demonstrated that de-differentiation as characterized by the induction of YAP1, FOXO3 and KRT17 was altered by ActA/TGFβ signaling. Collectively, our results suggest a pivotal role for ActA in the inflammatory GERD environment by modulating esophageal tissue repair and de-differentiation.

Indexed as

Cell DedifferentiationModels, BiologicalActivinsEpithelial CellsEsophagusGastroesophageal RefluxHumansactivin AActivinsBarrett’s esophagusGastroesophageal refluxInflammationStem cell markersTGFβ signaling

Identifiers

PMID31369967
PMCPMC6739184
OpenAlexW2964925642

What OpenQuestion holds

Textmetadata
LicenceTDM
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.