ArticleJournal of gastroenterology2011
Dissociation and dispersion of claudin-3 from the tight junction could be one of the most sensitive indicators of reflux esophagitis in a rat model of the disease.
Article in Journal of gastroenterology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- A randomized prospective study comparing the efficacy of on-demand therapy versus continuous therapy for 6 months for long-term maintenance with omeprazole 20 mg in patients with gastroesophageal reflux disease in Japan.Scandinavian journal of gastroenterology · 2014Trial
- The Prevention Effect of Lactobacillus plantarum 17-5 on Escherichia coli-Induced Mastitis in Mice.Probiotics and antimicrobial proteins · 2023Article
- NF-κB: A novel therapeutic pathway for gastroesophageal reflux disease?World journal of clinical cases · 2022Review
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- Comparison of Tight Junction Protein-Related Gene mRNA Expression Levels between Male and Female Gastroesophageal Reflux Disease Patients.Gut and liver · 2018Article
- Additive Effects of Rebamipide Plus Proton Pump Inhibitors on the Expression of Tight Junction Proteins in a Rat Model of Gastro-Esophageal Reflux Disease.Gut and liver · 2018Article
- Contribution of immunomodulators to gastroesophageal reflux disease and its complications: stromal cells, interleukin 4, and adiponectin.Annals of the New York Academy of Sciences · 2016Review
- Gastrointestinal mucosal barrier function and diseases.Journal of gastroenterology · 2016Review
- Biomarkers of Reflux Disease.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2016Review
- Estrogen Enhances Esophageal Barrier Function by Potentiating Occludin Expression.Digestive diseases and sciences · 2016Article
- Epithelial-derived nuclear IL-33 aggravates inflammation in the pathogenesis of reflux esophagitis.Journal of gastroenterology · 2015Article
- The degradation of airway tight junction protein under acidic conditions is probably mediated by transient receptor potential vanilloid 1 receptor.Bioscience reports · 2013Article
- Gastroesophageal reflux activates the NF-κB pathway and impairs esophageal barrier function in mice.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Esophageal intraluminal baseline impedance is associated with severity of acid reflux and epithelial structural abnormalities in patients with gastroesophageal reflux disease.Journal of gastroenterology · 2013Article
- Lipopolysaccharide disrupts the milk-blood barrier by modulating claudins in mammary alveolar tight junctions.PloS one · 2013Article
- Apical acidity decreases inhibitory effect of omeprazole on Mg(2+) absorption and claudin-7 and -12 expression in Caco-2 monolayers.Experimental & molecular medicine · 2012Article
- Role of tight junction proteins in gastroesophageal reflux disease.BMC gastroenterology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe aim of this study was to characterize pathological lesions of the esophageal epithelial tight junction (TJ) complex in a rat reflux esophagitis (RE) model in a search for a reliable diagnostic indicator.
methodsRats underwent an operation to induce RE, with or without rabeprazole treatment (1.0 and 10.0 mg/kg/day). Sham-operated rats served as a control. Fourteen days after the operation, esophagi were isolated from the rats and submitted to double-label confocal immunofluorescence microscopy, and biochemical analyses.
resultsImmunofluorescence microscopy revealed that claudins-1, -3, and -4 were located on the surfaces of epithelial cells in the normal esophagus of the control group, although there were differences in the distribution patterns between claudin-3 and claudins-1 and -4 in the epithelial layer. However, in RE, the immunoreactivity of claudin-3 on the cell surface was decreased, and it appeared instead as a faint granular pattern within the epithelial cytoplasm. Claudin-3 expression in the entire esophageal epithelium was also decreased. The expression and location of claudins-1 and -4 in epithelial cells were basically unaffected in RE. Gastric acid-induced dissociation of claudin-3 elicited instability of the epithelial TJ complex, which was confirmed by sedimentation analysis using centrifugation in a sucrose density gradient. Rabeprazole (10.0 mg/kg/day) attenuated these alterations.
conclusionsOur data indicate that the dispersion of claudin-3 from esophageal epithelial plasma membranes to cytoplasm and the resulting instability of the TJ complex could be one of the most specific and sensitive indicators for monitoring inflammatory and recovery processes in RE.
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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.