ArticleDigestive diseases and sciences2006
Omeprazole treatment ameliorates oxyntic atrophy induced by DMP-777.
Article in Digestive diseases and sciences, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Cellular lineage origins of spasmolytic polypeptide-expressing metaplasia (SPEM): persistent and intensifying debates.Frontiers in oncology · 2025Review
- Precancerous pathways to gastric cancer: a review of experimental animal models recapitulating the correa cascade.Frontiers in cell and developmental biology · 2025Review
- Role and research progress of spasmolytic polypeptide‑expressing metaplasia in gastric cancer (Review).International journal of oncology · 2024Article
- Role of spasmolytic polypeptide-expressing metaplasia in gastric mucosal diseases.American journal of cancer research · 2023Review
- Cellular Plasticity, Reprogramming, and Regeneration: Metaplasia in the Stomach and Beyond.Gastroenterology · 2022Review
- WFDC2 Promotes Spasmolytic Polypeptide-Expressing Metaplasia Through the Up-Regulation of IL33 in Response to Injury.Gastroenterology · 2021Article
- Tamoxifen Acts as a Parietal Cell Protonophore.Cellular and molecular gastroenterology and hepatology · 2020Article
- IL-10 Plays a Pivotal Role in Tamoxifen-Induced Spasmolytic Polypeptide-Expressing Metaplasia in Gastric Mucosa.Gut and liver · 2017Article
- Murine Models of Gastric Corpus Preneoplasia.Cellular and molecular gastroenterology and hepatology · 2017Review
- Loss of HGF activator inhibits foveolar hyperplasia induced by oxyntic atrophy without altering gastrin levels.American journal of physiology. Gastrointestinal and liver physiology · 2012Article
- Tamoxifen induces rapid, reversible atrophy, and metaplasia in mouse stomach.Gastroenterology · 2012Article
- The origin of pre-neoplastic metaplasia in the stomach: chief cells emerge from the Mist.Experimental cell research · 2011Review
- Oxyntic atrophy, metaplasia, and gastric cancer.Progress in molecular biology and translational science · 2010Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Atrophic gastritis, characterized as parietal cell loss or oxyntic atrophy, is the primary event in the evolution of the spectrum of metaplastic and hyperplastic lineage changes thought to predispose to gastric neoplasia. A number of animal models have provided insights into the lineage changes induced by oxyntic atrophy. Recently, we have reported a model for pharmacological induction of oxyntic atrophy with DMP-777. DMP-777 ablates parietal cells selectively and leads to the gastric cell lineage changes including foveolar hyperplasia and spasmolytic polypeptide expressing metaplasia (SPEM). Previous investigations showed that DMP-777 dissipated a gastric tubulovesicle proton gradient without impairing the H/K-ATPase activity, consistent with its pharmacological action as a parietal cell-specific protonophore which could induce parietal cell necrosis through backwash of luminal acid into actively secreting cells. We hypothesized that, if DMP-777 was acting as a parietal cell protonophore, then suppression of acid secretion should protect parietal cells from the toxic effects of the drug. In this study, we pretreated and coadministered the proton pump inhibitor omeprazole with DMP-777 to determine the effect of active acid secretion inhibition on the DMP-777-induced histologic changes in the stomachs of male rats. Omeprazole pretreatment ameliorated DMP-777-induced parietal cell loss as well as foveolar hyperplasia. These results indicate that active acid secretion is required for DMP-777 cytotoxicity, consistent with its suggested behavior as a parietal cell-specific protonophore.
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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.