ArticleCellular and molecular gastroenterology and hepatology2020
Hypergastrinemia Expands Gastric ECL Cells Through CCK2R
Article in Cellular and molecular gastroenterology and hepatology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 34 citations in OpenAlex.
- Gastrin-dependent expansion of Cck2rGut · 2026Article
- Perspectives on gastric cancer: the central role of gastrin in carcinogenesis byFrontiers in oncology · 2026Review
- Review
- Sleeve gastrectomy reveals the plasticity of the human gastric epithelium.Nature communications · 2025Article
- A Case of Brunner's Gland Hyperplasia Accompanied by an Increase in Endocrine Cells and Endocrine Cell Micronests.Cureus · 2024Article
- Omeprazole taken once every other day can effectively prevent aspirin-induced gastrointestinal mucosal damage in rats.BMC gastroenterology · 2024Article
- A novel telomere biology disease-associated gastritis identified through a whole exome sequencing-driven approach.The journal of pathology. Clinical research · 2024Article
- Neuroendocrine mechanism of gastric acid secretion: Historical perspectives and recent developments in physiology and pharmacology.Journal of neuroendocrinology · 2023Review
- Novel Insights into the Physiology of Nutrient Sensing and Gut-Brain Communication in Surgical and Experimental Obesity Therapy.Obesity surgery · 2023Review
- The composition and roles of gastric stem cells in epithelial homeostasis, regeneration, and tumorigenesis.Cellular oncology (Dordrecht, Netherlands) · 2023Review
- Gastric Stem Cell Biology and Helicobacter pylori Infection.Current topics in microbiology and immunology · 2023Article
- The central role of gastrin in gastric cancer.Frontiers in oncology · 2023Review
- Stem Cell Biomarkers and Tumorigenesis in Gastric Cancer.Journal of personalized medicine · 2022Review
- Gastric organoids: Advancing the study of H. pylori pathogenesis and inflammation.Helicobacter · 2022Review
- Review
- Gastrin: From Physiology to Gastrointestinal Malignancies.Function (Oxford, England) · 2022Review
- Gastrin/CCK-B Receptor Signaling Promotes Cell Invasion and Metastasis by Upregulating MMP-2 and VEGF Expression in Gastric Cancer.Journal of Cancer · 2022Article
- Chemoprevention of Oesophageal Squamous-Cell Carcinoma and Adenocarcinoma: A Multicentre Retrospective Cohort Study.Digestion · 2022Article
- Amelioration of alcohol‑induced gastric mucosa damage by oral administration of food‑polydeoxyribonucleotides.Molecular medicine reports · 2021Article
- Stem cells and origins of cancer in the upper gastrointestinal tract.Cell stem cell · 2021Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 4 countries.
Funding
Abstract
BACKGROUND &
aimsEnterochromaffin-like (ECL) cells in the stomach express gastrin/cholecystokinin 2 receptor CCK2R and are known to expand under hypergastrinemia, but whether this results from expansion of existing ECL cells or increased production from progenitors has not been clarified.
methodsWe used mice with green fluorescent protein fluorescent reporter expression in ECL cells (histidine decarboxylase [Hdc]-green fluorescent protein), as well as Cck2r- and Hdc-driven Tamoxifen inducible recombinase Cre (Cck2r-CreERT2, Hdc-CreERT2) mice combined with Rosa26Sor-tdTomato (R26-tdTomato) mice, and studied their expression and cell fate in the gastric corpus by using models of hypergastrinemia (gastrin infusion, omeprazole treatment).
resultsHdc-GFP marked the majority of ECL cells, located in the lower third of the gastric glands. Hypergastrinemia led to expansion of ECL cells that was not restricted to the gland base, and promoted cellular proliferation (Ki67) in the gastric isthmus but not in basal ECL cells. Cck2r-CreERT2 mice marked most ECL cells, as well as scattered cell types located higher up in the glands, whose number was increased during hypergastrinemia. Cck2r-CreERT2
conclusionsWe show here that hypergastrinemia induces ECL cell hyperplasia that is derived primarily from CCK2R
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