ArticleThe Journal of biological chemistry2008
Helicobacter pylori VacA disrupts apical membrane-cytoskeletal interactions in gastric parietal cells.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 73 citations in OpenAlex.
- Oxidative Phosphorylation System in Gastric Carcinomas and Gastritis.Oxidative medicine and cellular longevity · 2017Trial
- Antibiotics Impact the Cytotoxicity and Cytopathic Effect ofInternational journal of molecular sciences · 2025Article
- Vacuolating Cytotoxin A (VacA) and Extracellular Vesicles inIranian journal of pathology · 2025Review
- Modeling gastric intestinal metaplasia in 3D organoids using nitrosoguanidine.Journal of molecular cell biology · 2024Article
- Chromothripsis: an emerging crossroad from aberrant mitosis to therapeutic opportunities.Journal of molecular cell biology · 2024Review
- The immunopathogenesis ofFrontiers in microbiology · 2024Review
- Review
- Emerging role of human microbiome in cancer development and response to therapy: special focus on intestinal microflora.Journal of translational medicine · 2022Review
- Modeling of COVID-19 disease disparity in gastric organoids reveals the spatiotemporal dynamics of SARS-CoV-2 infectivity.Journal of molecular cell biology · 2022Article
- Review
- Functional Properties of Oligomeric and Monomeric Forms of Helicobacter pylori VacA Toxin.Infection and immunity · 2021Article
- Gut Microbiota in Lung Cancer: Where Do We Stand?International journal of molecular sciences · 2021Review
- Potent antitumor activity of a glutamyltransferase-derived peptide via an activation of oncosis pathway.Scientific reports · 2021Article
- Plasma membrane integrity: implications for health and disease.BMC biology · 2021Review
- Chronic in vivo exposure to Helicobacter pylori VacA: Assessing the efficacy of automated and long-term intragastric toxin infusion.Scientific reports · 2020Article
- Risk factors associated with gastric malignancy during chronicMedical research archives · 2020Article
- Gastric Parietal Cell Physiology and Helicobacter pylori-Induced Disease.Gastroenterology · 2019Review
- Review
- MST4 kinase phosphorylates ACAP4 protein to orchestrate apical membrane remodeling during gastric acid secretion.The Journal of biological chemistry · 2017Article
- The role of the microbiome in cancer development and therapy.CA: a cancer journal for clinicians · 2017Review
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Authors and funding
19 authors at 6 institutions in 2 countries.
Funding
Abstract
Helicobacter pylori persistently colonize the human stomach and have been linked to atrophic gastritis and gastric carcinoma. Although it is well known that H. pylori infection can result in hypochlorhydria, the molecular mechanisms underlying this phenomenon remain poorly understood. Here we show that VacA permeabilizes the apical membrane of gastric parietal cells and induces hypochlorhydria. The functional consequences of VacA infection on parietal cell physiology were studied using freshly isolated rabbit gastric glands and cultured parietal cells. Secretory activity of parietal cells was judged by an aminopyrine uptake assay and confocal microscopic examination. VacA permeabilization induces an influx of extracellular calcium, followed by activation of calpain and subsequent proteolysis of ezrin at Met(469)-Thr(470), which results in the liberation of ezrin from the apical membrane of the parietal cells. VacA treatment inhibits acid secretion by preventing the recruitment of H,K-ATPase-containing tubulovesicles to the apical membrane of gastric parietal cells. Electron microscopic examination revealed that VacA treatment disrupts the radial arrangement of actin filaments in apical microvilli due to the loss of ezrin integrity in parietal cells. Significantly, expression of calpain-resistant ezrin restored the functional activity of parietal cells in the presence of VacA. Proteolysis of ezrin in VacA-infected parietal cells is a novel mechanism underlying H. pylori-induced inhibition of acid secretion. Our results indicate that VacA disrupts the apical membrane-cytoskeletal interactions in gastric parietal cells and thereby causes hypochlorhydria.
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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.