ArticleCellular and molecular gastroenterology and hepatology2021
Claudin-18 Loss Alters Transcellular Chloride Flux but not Tight Junction Ion Selectivity in Gastric Epithelial Cells.
Article in Cellular and molecular gastroenterology and hepatology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Claudin-18.2: Molecular mechanisms to clinical translation in solid tumors (Review).Oncology letters · 2026Review
- Clinicopathological and molecular mechanisms of CLDN18.2 in gastric cancer aggressiveness: a high-risk population study with multi-omics profiling.Journal of pathology and translational medicine · 2026Article
- Genetically engineered mouse models in gastric precancerous lesions research.World journal of gastrointestinal surgery · 2025Review
- The preclinical discovery and development of zolbetuximab for the treatment of gastric cancer.Expert opinion on drug discovery · 2024Review
- Zolbetuximab for Claudin18.2-positive gastric or gastroesophageal junction cancer.Therapeutic advances in medical oncology · 2024Review
- Expression and Targeted Application of Claudins Family in Hepatobiliary and Pancreatic Diseases.Journal of hepatocellular carcinoma · 2024Review
- Pharmacological targeting of gastric mucosal barrier with traditional Chinese medications for repairing gastric mucosal injury.Frontiers in pharmacology · 2023Review
- Redox and Metabolic Regulation of Intestinal Barrier Function and Associated Disorders.International journal of molecular sciences · 2022Review
- Claudin18.2 is a novel molecular biomarker for tumor-targeted immunotherapy.Biomarker research · 2022Review
- Context-Dependent Roles of Claudins in Tumorigenesis.Frontiers in oncology · 2021Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
BACKGROUND &
aimsTight junctions form a barrier to the paracellular passage of luminal antigens. Although most tight junction proteins reside within the apical tight junction complex, claudin-18 localizes mainly to the basolateral membrane where its contribution to paracellular ion transport is undefined. Claudin-18 loss in mice results in gastric neoplasia development and tumorigenesis that may or may not be due to tight junction dysfunction. The aim here was to investigate paracellular permeability defects in stomach mucosa from claudin-18 knockout (Cldn18-KO) mice.
methodsStomach tissue from wild-type, heterozygous, or Cldn18-KO mice were stripped of the external muscle layer and mounted in Ussing chambers. Transepithelial resistance, dextran 4 kDa flux, and potential difference (PD) were calculated from the chambered tissues after identifying differences in tissue histopathology that were used to normalize these measurements. Marker expression for claudins and ion transporters were investigated by transcriptomic and immunostaining analysis.
resultsNo paracellular permeability defects were evident in stomach mucosa from Cldn18-KO mice. RNAseq identified changes in 4 claudins from Cldn18-KO mice, particularly the up-regulation of claudin-2. Although claudin-2 localized to tight junctions in cells at the base of gastric glands, its presence did not contribute overall to mucosal permeability. Stomach tissue from Cldn18-KO mice also had no PD versus a lumen-negative PD in tissues from wild-type mice. This difference resulted from changes in transcellular Cl
conclusionsOur findings suggest that Cldn18-KO has no effect on tight junction permeability in the stomach from adult mice but rather affects anion permeability. The phenotype in these mice may thus be secondary to transcellular anion transporter expression/function in the absence of claudin-18.
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