ArticleGut2007
Retinoic acid-induced glandular differentiation of the oesophagus.
Article in Gut, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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.
Who cites it
32 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.
- Treatment for Barrett's oesophagus.The Cochrane database of systematic reviews · 2010Pooled it
- Epithelial architecture and signaling activity in the adult human esophagus.Frontiers in cell and developmental biology · 2025Review
- Intrinsic Cellular Susceptibility to Barrett's Esophagus in Adults Born with Esophageal Atresia.Cancers · 2022Article
- Origins of Metaplasia in the Esophagus: Is This a GE Junction Stem Cell Disease?Digestive diseases and sciences · 2018Review
- The Microenvironment in Barrett's Esophagus Tissue Is Characterized by HighFrontiers in immunology · 2018Article
- Esophageal 3D Culture Systems as Modeling Tools in Esophageal Epithelial Pathobiology and Personalized Medicine.Cellular and molecular gastroenterology and hepatology · 2018Review
- Porcine Esophageal Submucosal Gland Culture Model Shows Capacity for Proliferation and Differentiation.Cellular and molecular gastroenterology and hepatology · 2017Article
- Oesophageal Stem Cells and Cancer.Advances in experimental medicine and biology · 2017Article
- Mechanisms of Barrett's oesophagus: intestinal differentiation, stem cells, and tissue models.Best practice & research. Clinical gastroenterology · 2015Review
- Article
- Barrett oesophagus: lessons on its origins from the lesion itself.Nature reviews. Gastroenterology & hepatology · 2015Review
- Cellular heterogeneity in the mouse esophagus implicates the presence of a nonquiescent epithelial stem cell population.Cell reports · 2014Article
- Modeling human gastrointestinal inflammatory diseases using microphysiological culture systems.Experimental biology and medicine (Maywood, N.J.) · 2014Review
- Barrett esophagus: history, definition and etiopathogeny.Journal of medicine and life · 2014Review
- Retinoic acid suppresses intestinal mucus production and exacerbates experimental enterocolitis.Disease models & mechanisms · 2012Article
- Development and characterization of an organotypic model of Barrett's esophagus.Journal of cellular physiology · 2012Article
- Review: Experimental models for Barrett's esophagus and esophageal adenocarcinoma.American journal of physiology. Gastrointestinal and liver physiology · 2012Review
- Barrett's Esophagus: Emerging Knowledge and Management Strategies.Pathology research international · 2012Article
- Cyclooxygenase-2 expression in esophageal epithelium before and after photodynamic therapy for Barrett's esophagus with high-grade dysplasia or intramucosal carcinoma.Virchows Archiv : an international journal of pathology · 2011Article
- Molecular mechanisms of Barrett's esophagus.Digestive diseases and sciences · 2011Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundRetinoic acid (RA) is a powerful differentiation agent. Barrett's oesophagus occurs when duodeno-gastro-oesophageal reflux causes squamous epithelium (SE) tissue to become columnar epithelium tissue by an unknown mechanism. The bile acid lithocholic acid (LCA) competes for the retinoid X receptor retinoid binding site. Hence, RA pathways may be implicated in Barrett's oesophagus.
methodsRA activity in tissues and cell lines treated with all-trans retinoic acid (ATRA) with or without LCA was assessed using a reporter. Expression of p21 was determined by real-time PCR in Barrett's oesophagus cell lines with or without LCA. SE and Barrett's oesophagus biopsy specimens were exposed to 100 muM of ATRA or 20 mM of a RA inhibitor, citral, in organ culture for >72 h. Characteristics of treated specimens, compared with untreated controls, were analysed by immunohistochemical analysis (cytokeratins (CKs), vimentin) and RT-PCR (CKs). Confocal microscopy assessed temporal changes in co-localisation of CK8/18 and vimentin. Cell proliferation was assessed by bromo-deoxyuridine incorporation and immunohistochemical analysis for Ki67 and p21.
resultsRA biosynthesis was increased in Barrett's oesophagus compared with SE (p<0.001). LCA and ATRA caused a synergistic increase in RA signalling as shown by increased p21 (p<0.01). Morphological and molecular analysis of SE exposed to ATRA showed columnar differentiation independent of proliferation. Metaplasia could be induced from the stromal compartment alone and vimentin expression co-localised with CK8/18 at 24 h, which separated into CK8/18-positive glands and vimentin-positive stroma by 48 h. Citral-treated Barrett's oesophagus led to phenotypic and immunohistochemical characteristics of SE, which was independent of proliferation.
conclusionRA activity is increased in Barrett's oesophagus and is induced by LCA. Under conditions of altered RA activity and an intact stroma, the oesophageal phenotype can be altered independent of proliferation.
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Registered trials
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.