ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012
Acetaldehyde disrupts tight junctions in Caco-2 cell monolayers by a protein phosphatase 2A-dependent mechanism.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 64 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
64 citing papers in PubMed, 1 synthesis or guideline pooled it, 97 citations in OpenAlex.
- ALDH2 and ADH1 genetic polymorphisms may contribute to the risk of gastric cancer: a meta-analysis.PloS one · 2014Pooled it
- Ethanol, acetaldehyde, lipopolysaccharide, and neutrophil extracellular traps: four-pronged attack on gut epithelial barrier in alcohol use disorder.Anatomical record (Hoboken, N.J. : 2007) · 2026Review
- Macrophage-derived cathepsin B disrupts intestinal tight junctions through occludin degradation and promotes alcohol-associated liver disease.Journal of hepatology · 2026Article
- The Multifaceted Roles of Gut Microbiota and Their Metabolites in Metabolic Dysfunction-associated Steatotic Liver Disease: A Literature Review.Journal of clinical and translational hepatology · 2026Review
- The gut mycobiome and inter-kingdom microbial networks are linked to COPD severity in lung cancer patients.Scientific reports · 2026Article
- The gut-brain axis as a therapeutic target in alcohol use disorder: dietary fiber, intestinal barrier integrity, and neuroinflammatory mechanisms underlying depression.Frontiers in nutrition · 2026Article
- Betaine supplementation prevents ethanol-induced disruption of intestinal tight junction integrity and liver inflammation in rats.Biochemical and biophysical research communications · 2026Article
- Advances in the acting mechanism and treatment of gut microbiota in metabolic dysfunction-associated steatotic liver disease.Gut microbes · 2025Review
- Article
- A three-dimensional high throughput assay identifies novel antibacterial molecules with activity against intracellular Shigella.npj antimicrobials and resistance · 2025Article
- Alcohol-induced gut permeability defect through dysbiosis and enterocytic mitochondrial interference causing pro-inflammatory macrophages in a dose dependent manner.Scientific reports · 2025Article
- Gut microbiota modulation by Traditional Chinese Medicine: a translational strategy for metabolic dysfunction-associated steatotic liver disease.Frontiers in pharmacology · 2025Review
- Urolithin A regulates gut: liver axis to ameliorate alcohol-associated liver disease.Frontiers in pharmacology · 2025Article
- Betaine regulates the gut-liver axis: a therapeutic approach for chronic liver diseases.Frontiers in nutrition · 2025Review
- Elafibranor alleviates alcohol-related liver fibrosis by restoring intestinal barrier function.World journal of gastroenterology · 2024Article
- Probiotics as Potential Therapeutic Agents: Safeguarding Skeletal Muscle against Alcohol-Induced Damage through the Gut-Liver-Muscle Axis.Biomedicines · 2024Review
- The involvement of oral bacteria in inflammatory bowel disease.Gastroenterology report · 2024Review
- Okadaic Acid Is at Least as Toxic as Dinophysistoxin-1 after Repeated Administration to Mice by Gavage.Toxins · 2023Article
- New Insights into the Pathogenesis of Metabolic-Associated Fatty Liver Disease (MAFLD): Gut-Liver-Heart Crosstalk.Nutrients · 2023Review
- Fermentation Supernatant of Elderly Feces with Inulin and Partially Hydrolyzed Guar Gum Maintains the Barrier of Inflammation-Induced Caco-2/HT29-MTX-E12 Co-Cultured Cells.Journal of agricultural and food chemistry · 2023Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Acetaldehyde is accumulated at high concentrations in the colonic lumen following ethanol administration. Previous studies demonstrated that acetaldehyde disrupts intestinal epithelial tight junctions and increases paracellular permeability. In the present study, we investigated the role of PP2A in the acetaldehyde-induced disruption of intestinal epithelial tight junctions. Caco-2 cell monolayers were exposed to 200-600 μM acetaldehyde for varying times, and the epithelial barrier function was evaluated by measuring transepithelial electrical resistance and inulin permeability. Acetaldehyde treatment resulted in a time-dependent increase in inulin permeability and redistribution of occludin and ZO-1 from the intercellular junctions. Treatment of cells with fostriecin (a PP2A-selective inhibitor) or knockdown of PP2A by siRNA blocked acetaldehyde-induced increase in inulin permeability and redistribution of occludin and ZO-1. The effects of fostriecin and acetaldehyde were confirmed in mouse intestine ex vivo. Acetaldehyde-induced tight junction disruption and barrier dysfunction were also attenuated by a PP2A-specific inhibitory peptide, TPDYFL. Coimmunoprecipitation studies showed that acetaldehyde increased the interaction of PP2A with occludin and induced dephosphorylation of occludin on threonine residues. Fostriecin and TPDYFL significantly reduced acetaldehyde-induced threonine dephosphorylation of occludin. Acetaldehyde failed to change the level of the methylated form of PP2A-C subunit. However, genistein (a tyrosine kinase inhibitor) blocked acetaldehyde-induced association of PP2A with occludin and threonine dephosphorylation of occludin. These results demonstrate that acetaldehyde-induced disruption of tight junctions is mediated by PP2A translocation to tight junctions and dephosphorylation of occludin on threonine residues.
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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.