Evidence map›Paper›PMID 28935573›Full record

ArticleThe American journal of pathology2017

Acrolein Disrupts Tight Junction Proteins and Causes Endoplasmic Reticulum Stress-Mediated Epithelial Cell Death Leading to Intestinal Barrier Dysfunction and Permeability.

Wei-Yang Chen, Min Wang, Jingwen Zhang, Shirish S Barve, Craig J McClain, Swati Joshi-Barve

Open access · bronzeAbstract read
In one paragraph

Article in The American journal of pathology, 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
4.3field-weighted citation impact, top 5% 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, 102 citations in OpenAlex.

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  13. The Role of Vitamins in Spinal Cord Injury: Mechanisms and Benefits.Oxidative medicine and cellular longevity · 2024
    Review
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  18. Frontiers in microbiomes · 2023
    Article
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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

6 authors at 1 institution in 1 country.

Wei-Yang ChenDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, Kentucky; Alcohol Research Center, University of Louisville, Louisville, Kentucky.
Min WangAlcohol Research Center, University of Louisville, Louisville, Kentucky; Department of Medicine, University of Louisville, Louisville, Kentucky; Hepatobiology and Toxicology Center, University of Louisville, Louisville, Kentucky.
Jingwen ZhangAlcohol Research Center, University of Louisville, Louisville, Kentucky; Department of Medicine, University of Louisville, Louisville, Kentucky; Hepatobiology and Toxicology Center, University of Louisville, Louisville, Kentucky.
Shirish S BarveDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, Kentucky; Alcohol Research Center, University of Louisville, Louisville, Kentucky; Department of Medicine, University of Louisville, Louisville, Kentucky; Hepatobiology and Toxicology Center, University of Louisville, Louisville, Kentucky.
Craig J McClainDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, Kentucky; Alcohol Research Center, University of Louisville, Louisville, Kentucky; Department of Medicine, University of Louisville, Louisville, Kentucky; Hepatobiology and Toxicology Center, University of Louisville, Louisville, Kentucky; Department of Medicine, Robley Rex Veterans Affairs Medical Center, Louisville, Kentucky.
Swati Joshi-BarveDepartment of Pharmacology and Toxicology, University of Louisville, Louisville, Kentucky; Alcohol Research Center, University of Louisville, Louisville, Kentucky; Department of Medicine, University of Louisville, Louisville, Kentucky; Hepatobiology and Toxicology Center, University of Louisville, Louisville, Kentucky. Electronic address: s0josh01@louisville.edu.
University of Louisville · US

Funding

Role of oxidized linoleic acid metabolites in the pathogenesis of alcoholic liver diseaseP20GM113226 · NIGMS · UNIVERSITY OF LOUISVILLE · PI BARVE, SHIRISH S · 2016 to 2025
$24.1M
The Role of Nutrition in the Development/Progression of Alcohol-Induced Organ InjuryP50AA024337 · NIAAA · UNIVERSITY OF LOUISVILLE · PI SHIRISH S BARVE · 2016 to 2026
$17.9M
Novel Therapies for Alcoholic HepatitisU01AA021893 · NIAAA · CLEVELAND CLINIC LERNER COM-CWRU · PI MCCLAIN, CRAIG J., MCCULLOUGH, ARTHUR JOSEPH · 2012 to 2017
$6.0M
Oxidized Metabolites of Linoleic Acid in Alcohol-induced Liver InjuryU01AA022489 · NIAAA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI FELDSTEIN, ARIEL, MCCLAIN, CRAIG J. · 2014 to 2018
$1.7M
Cyclic AMP, Cytokine Modulation and Alcoholic Liver DiseaseR01AA018869 · NIAAA · UNIVERSITY OF LOUISVILLE · PI MCCLAIN, CRAIG J. · 2009 to 2013
$1.7M
Mechanisms for alcohol induced gut barrier dysfunction in ALDR01AA023681 · NIAAA · UNIVERSITY OF LOUISVILLE · PI MCCLAIN, CRAIG J. · 2014 to 2018
$1.6M
SAM Deficiency Mediated Epigenetic Mechanisms in Alcohol induced ImmunosuppressionR01AA024405 · NIAAA · UNIVERSITY OF LOUISVILLE · PI BARVE, SHIRISH S · 2015 to 2019
$1.6M
Novel therapies in alcoholic hepatitis University of LouisvilleU01AA021901 · NIAAA · UNIVERSITY OF LOUISVILLE · PI MCCLAIN, CRAIG J. · 2012 to 2017
$1.5M
Ubiquitous pollutant acrolein inhibits IFN?? antiviral signaling: relevance to HCK01ES017105 · NIEHS · UNIVERSITY OF LOUISVILLE · PI JOSHI-BARVE, SWATI · 2010 to 2014
$655k
Dietary Fat and Alcoholic Liver DiseaseI01BX002996 · VA · LOUISVILLE VA MEDICAL MEDICAL CENTER · PI MCCLAIN, CRAIG J. · 2017 to 2020
–
BLRD VA I01 BX002996NIAAA NIH HHS P50 AA024337NIAAA NIH HHS R01 AA018869NIAAA NIH HHS R01 AA023681NIAAA NIH HHS R01 AA024405NIAAA NIH HHS U01 AA021893NIAAA NIH HHS U01 AA021901NIAAA NIH HHS U01 AA022489NIEHS NIH HHS K01 ES017105NIGMS NIH HHS P20 GM113226
6 · The paper itself

Abstract

Increasing evidence suggests that environmental and dietary factors can affect intestinal epithelial integrity leading to gut permeability and bacterial translocation. Intestinal barrier dysfunction is a pathogenic process associated with many chronic disorders. Acrolein is an environmental and dietary pollutant and a lipid-derived endogenous metabolite. The impact of acrolein on the intestine has not been investigated before and is evaluated in this study, both in vitro and in vivo. Our data demonstrate that oral acrolein exposure in mice caused damage to the intestinal epithelial barrier, resulting in increased permeability and subsequently translocation of bacterial endotoxin-lipopolysaccharide into the blood. Similar results were seen in vitro using established Caco-2 cell monolayers wherein acrolein decreased barrier function and increased permeability. Acrolein also caused the down-regulation and/or redistribution of three representative tight junction proteins (ie, zonula occludens-1, Occludin, Claudin-1) that critically regulate epithelial paracellular permeability. In addition, acrolein induced endoplasmic reticulum stress-mediated death of epithelial cells, which is an important mechanism contributing to intestinal barrier damage/dysfunction, and gut permeability. Overall, we demonstrate that exposure to acrolein affects the intestinal epithelium by decrease/redistribution of tight junction proteins and endoplasmic reticulum stress-mediated epithelial cell death, thereby resulting in loss of barrier integrity and function. Our findings highlight the adverse consequences of environmental and dietary pollutants on intestinal barrier integrity/function with relevance to gut permeability and the development of disease.

Indexed as

AcroleinAnimalsApoptosisCaco-2 CellsEndoplasmic Reticulum StressHumansIntestinal MucosaMaleMiceMice, Inbred C57BLPermeabilityTight Junction ProteinsAcroleinTight Junction Proteins

Identifiers

PMID28935573
PMCPMC5818631
OpenAlexW2755291309

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.