ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2011
Characterization of squamous esophageal cells resistant to bile acids at acidic pH: implication for Barrett's esophagus pathogenesis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 1 of them a synthesis that pooled it.
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Who cites it
21 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.
- Cell culture models for studying the development of Barrett's esophagus: a systematic review.Cellular oncology (Dordrecht, Netherlands) · 2012Pooled it
- Effects of phenytoin on ethanol-induced gastric ulceration in rats: involvement of oxidative stress, inflammation, and apoptosis.Journal of pharmaceutical health care and sciences · 2026Article
- Optimal cannabinoid-terpene combination ratios suppress mutagenicity of gastric reflux in normal and metaplastic esophageal cells.World journal of gastroenterology · 2026Article
- The potential protective mechanisms of melatonin on alcoholic fatty liver disease based on the animal study.Frontiers in veterinary science · 2026Article
- Impact of Cholecystectomy on Gastric Mucosal c-MYC and h-TERT Expression; A Potential Link to Gastric Cancer Development.Balkan journal of medical genetics : BJMG · 2025Article
- The role of the fibroblast in Barrett's esophagus and esophageal adenocarcinoma.Current opinion in gastroenterology · 2024Review
- Research progress of cancer stem cells and IL-6/STAT3 signaling pathway in esophageal adenocarcinoma.Translational cancer research · 2020Review
- Activin A-mediated epithelial de-differentiation contributes to injury repair in an in vitro gastrointestinal reflux model.Cytokine · 2019Article
- The cyclical hit model: how paligenosis might establish the mutational landscape in Barrett's esophagus and esophageal adenocarcinoma.Current opinion in gastroenterology · 2019Review
- microRNA involvement in the onset and progression of Barrett's esophagus: a systematic review.Oncotarget · 2018Review
- Medical Conditions in the First Years of Life Associated with Future Diagnosis of ASD in Children.Journal of autism and developmental disorders · 2017Article
- Role of nitric oxide in the pathogenesis of Barrett's-associated carcinogenesis.World journal of gastrointestinal pathophysiology · 2016Review
- Article
- Control of acid and duodenogastroesophageal reflux (DGER) in patients with Barrett's esophagus.The American journal of gastroenterology · 2015Article
- Differential regulation of EGFR-MAPK signaling by deoxycholic acid (DCA) and ursodeoxycholic acid (UDCA) in colon cancer.Digestive diseases and sciences · 2014Review
- NFkB and Nrf2 in esophageal epithelial barrier function.Tissue barriers · 2013Article
- Alcohol is an oxidative stressor for gastric epithelial cells: detection of superoxide in living cells.Journal of clinical biochemistry and nutrition · 2013Article
- Gastroesophageal reflux activates the NF-κB pathway and impairs esophageal barrier function in mice.American journal of physiology. Gastrointestinal and liver physiology · 2013Article
- Role of epidermal growth factor receptor tyrosine kinase inhibitors in the treatment of esophageal carcinoma and the suggested mechanisms of action.Oncology letters · 2013Article
- Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Barrett's esophagus (BE) is a premalignant condition, where normal squamous epithelium is replaced by intestinal epithelium. BE is associated with an increased risk of developing esophageal adenocarcinoma (EAC). However, the BE cell of origin is not clear. We hypothesize that BE tissue originates from esophageal squamous cells, which can differentiate to columnar cells as a result of repeated exposure to gastric acid and bile acids, two components of refluxate implicated in BE pathology. To test this hypothesis, we repeatedly exposed squamous esophageal HET1A cells to 0.2 mM bile acid (BA) cocktail at pH 5.5 and developed an HET1AR-resistant cell line. These cells are able to survive and proliferate after repeated 2-h treatments with BA at pH 5.5. HET1AR cells are resistant to acidification and express markers of columnar differentiation, villin, CDX2, and cytokeratin 8/18. HET1AR cells have increased amounts of reactive oxygen species, concomitant with a decreased level and activity of manganese superoxide dismutase compared with parental cells. Furthermore, HET1AR cells express proteins and activate signaling pathways associated with inflammation, cell survival, and tumorigenesis that are thought to contribute to BE and EAC development. These include STAT3, NF-κB, epidermal growth factor receptor (EGFR), cyclooxygenase-2, interleukin-6, phosphorylated mammalian target of rapamycin (p-mTOR), and Mcl-1. The expression of prosurvival and inflammatory proteins and resistance to cell death could be partially modified by inhibition of STAT3 signaling. In summary, our study shows that long-term exposure of squamous cells to BA at acidic pH causes the cells to display the same characteristics and markers as BE.
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