ArticlePhilosophical transactions of the Royal Society of London. Series B, Biological sciences2016
The zinc sensing receptor, ZnR/GPR39, triggers metabotropic calcium signalling in colonocytes and regulates occludin recovery in experimental colitis.
Article in Philosophical transactions of the Royal Society of London. Series B, Biological sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.
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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.
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Who cites it
26 citing papers in PubMed, 50 citations in OpenAlex.
- GPR39 activation inhibits AQP2 trafficking and alters cytoskeletal organization.American journal of physiology. Cell physiology · 2026Article
- GPR39 Suppresses Ferroptosis via the Nrf2/SLC7A11 Axis and Reduces the Sensitivity of Colorectal Cancer to Anti-PD-1 Immunotherapy.Canadian journal of gastroenterology & hepatology · 2026Article
- Loss of the zinc receptor ZnR/GPR39 in mice enhances anxiety-related behavior and motor deficits, and modulates KCC2 expression in the amygdala.Behavioral and brain functions : BBF · 2024Article
- Zinc Deficiency and Zinc Supplementation in Allergic Diseases.Biomolecules · 2024Review
- Signaling pathway mechanisms of neurological diseases induced by G protein-coupled receptor 39.CNS neuroscience & therapeutics · 2023Review
- Tight junctions: from molecules to gastrointestinal diseases.Tissue barriers · 2023Article
- Preparation and characterization of garlic polysaccharide-Zn (II) complexes and their bioactivities as a zinc supplement in Zn-deficient mice.Food chemistry: X · 2022Article
- Functions of the Zinc-Sensing Receptor GPR39 in Regulating Intestinal Health in Animals.International journal of molecular sciences · 2022Review
- The Impact of Zinc and Zinc Homeostasis on the Intestinal Mucosal Barrier and Intestinal Diseases.Biomolecules · 2022Review
- Article
- Activation of GPR39 with TC-G 1008 attenuates neuroinflammation via SIRT1/PGC-1α/Nrf2 pathway post-neonatal hypoxic-ischemic injury in rats.Journal of neuroinflammation · 2021Article
- Zinc Signaling in the Mammary Gland: For Better and for Worse.Biomedicines · 2021Review
- Role of GPR39 in Neurovascular Homeostasis and Disease.International journal of molecular sciences · 2021Review
- The Zinc-Sensing Receptor GPR39 in Physiology and as a Pharmacological Target.International journal of molecular sciences · 2021Review
- Paracellular Filtration Secretion Driven by Mechanical Force Contributes to Small Intestinal Fluid Dynamics.Medical sciences (Basel, Switzerland) · 2021Article
- Targeting of G-protein coupled receptors in sepsis.Pharmacology & therapeutics · 2020Review
- Maintenance of Intestinal Epithelial Homeostasis by Zinc Transporters.Digestive diseases and sciences · 2019Review
- Modulation of Gpr39, a G-protein coupled receptor associated with alcohol use in non-human primates, curbs ethanol intake in mice.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- Contribution of Zinc and Zinc Transporters in the Pathogenesis of Inflammatory Bowel Diseases.Journal of immunology research · 2019Review
- Enhanced ZnR/GPR39 Activity in Breast Cancer, an Alternative Trigger of Signaling Leading to Cell Growth.Scientific reports · 2018Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors at 1 institution in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Impaired epithelial barrier function is a hallmark of inflammatory bowel diseases, such as colitis, contributing to diarrhoea and perpetuating inflammation. We show that the zinc sensing receptor, ZnR/GPR39, triggers intracellular Ca(2+) signalling in colonocytes thereby inducing occludin expression. Moreover, ZnR/GPR39 is essential for epithelial barrier recovery in the dextran sodium sulfate (DSS) ulcerative colitis model. Loss of ZnR/GPR39 results in increased susceptibility to DSS-induced inflammation, owing to low expression of the tight junction protein occludin and impaired epithelial barrier. Recovery of wild-type (WT) mice from the DSS insult was faster than that of ZnR/GPR39 knockout (KO) mice. Enhanced recovery of the epithelial layer and increased crypt regeneration were observed in WT mice compared with ZnR/GPR39 KO, suggesting that ZnR/GPR39 is promoting epithelial barrier integrity following DSS insult. Indeed, cell proliferation and apical expression of occludin, following the DSS-induced epithelial erosion, were increased in WT tissue but not in ZnR/GPR39 KO tissue. Importantly, survival following DSS treatment was higher in WT mice compared with ZnR/GPR39 KO mice. Our results support a direct role for ZnR/GPR39 in promoting epithelial renewal and barrier function following DSS treatment, thereby affecting the severity of the disease. We suggest ZnR/GPR39 as a novel therapeutic target that can improve epithelial barrier function in colitis.This article is part of the themed issue 'Evolution brings Ca(2+) and ATP together to control life and death'.
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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.