ArticleScientific reports2017
Chronic stress and intestinal barrier dysfunction: Glucocorticoid receptor and transcription repressor HES1 regulate tight junction protein Claudin-1 promoter.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 91 citations in OpenAlex.
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- Unveiling the enigma of anxiety disorders and depression: from pathogenesis to treatment.Science China. Life sciences · 2026Review
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- Microbial regulation of stress-associated signaling molecules and its role in health and disease.NPJ biofilms and microbiomes · 2026Review
- Modulation of SIRT1/PPARγ pathways and tight junction proteins by nicotinamide riboside under chronic variable stress.Journal of physiology and biochemistry · 2026Article
- Gut microbiota dysbiosis at the interface of neuropsychiatric disorders and their dermatological comorbidities.Gut microbes · 2025Review
- Navigating mental health in space: gut-brain axis and microbiome dynamics.Experimental & molecular medicine · 2025Review
- Novel hypothesis and therapeutic interventions for irritable bowel syndrome: interplay between metal dyshomeostasis, gastrointestinal dysfunction, and neuropsychiatric symptoms.Molecular and cellular biochemistry · 2025Review
- Effect of heat stress on ileal epithelial barrier integrity in broilers divergently selected for high- and low-water efficiency.Frontiers in physiology · 2025Article
- Microbial orchestration of neuroimmune crosstalk: from homeostasis to disease.Frontiers in immunology · 2025Review
- Gut-Brain Axis: Role of Microbiome, Metabolomics, Hormones, and Stress in Mental Health Disorders.Cells · 2024Review
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- Water Avoidance-Stress Induces Differential Colon Transcriptomic Responses in BALB/c and C57BL/6 Mice Irritable Bowel Syndrome Model.Gastro hep advances · 2024Review
- Acute stress triggers sex-dependent rapid alterations in the human small intestine microbiota composition.Frontiers in microbiology · 2024Article
- Decreasing the steroid rapidly may help to improve the clinical outcomes of patients with intestinal steroid-refractory acute graft-versus-host disease receiving basiliximab treatment.Frontiers in oncology · 2024Article
- Role of Stress on Driving the Intestinal Paracellular Permeability.Current issues in molecular biology · 2023Review
- Glucocorticoid receptor-mediatediScience · 2023Article
- Ezrin accelerates breast cancer liver metastasis through promoting furin-like convertase-mediated cleavage of Notch1.Cellular oncology (Dordrecht, Netherlands) · 2023Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Chronic stress and elevated glucocorticoid hormone are associated with decreases in the intestinal epithelial tight junction protein claudin-1 (CLDN1). Human/rat CLDN1 promoters contain glucocorticoid response elements (GREs) and adjacent transcription repressor HES1 binding N-boxes. Notch signaling target HES1 expression was high and glucocorticoid receptor (NR3C1) low at the crypt base and the pattern reversed at the crypt apex. Chronic stress reduced overall rat colon HES1 and NR3C1 that was associated with CLDN1 downregulation. Chromatin-immunoprecipitation experiments showed that HES1 and NR3C1 bind to the CLDN1 promoter in rat colon crypts. The binding of NR3C1 but not HES1 to CLDN1 promoter significantly decreased in chronically stressed animals, which was prevented by the NR3C1 antagonist RU486. We employed the 21-day Caco-2/BBe cell model to replicate cell differentiation along the crypt axis. HES1 siRNA treatment early in differentiation increased CLDN1. In contrast, stress levels of cortisol decreased CLDN1 in late differentiation stage but not in the early stage. HES1 was high, whereas NR3C1 and CLDN1 were low in the early stage which reversed in the late stage, e.g. HES1/NR3C1 binding to CLDN1 promoter demonstrates a dynamic and reciprocal pattern. These results suggest that chronic stress impairs colon epithelium homeostasis and barrier function via different mechanisms along the crypt axis.
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