ArticleAmerican journal of physiology. Cell physiology2015
Tumor necrosis factor-α induces a biphasic change in claudin-2 expression in tubular epithelial cells: role in barrier functions.
Article in American journal of physiology. Cell physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 50 citations in OpenAlex.
- Inflammation-Induced Claudin-2 Up-Regulation Limits Pancreatitis Development by Enhancing Pancreatic Ductal Transport.Gastroenterology · 2026Article
- The Degree of Liver Steatosis Is Associated with Abnormally High Serum Levels of Markers of Blood-Brain Barrier Dysfunction and Systemic Inflammation in Patients with Morbid Obesity.Medicina (Kaunas, Lithuania) · 2026Article
- Indole-3-Acetic Acid and Skatole Exert Opposing Effects on MDR1 Proteostasis in Human Colonic Epithelial Cells: A Molecular Basis for the Gut Microbial Metabolic Switch.Journal of xenobiotics · 2026Article
- Capsaicin attenuates the effect of inflammatory cytokines in a HaCaT cell model for basal keratinocytes.Frontiers in pharmacology · 2024Article
- Claudin-2 Mediates the Proximal Tubular Epithelial Cell-Fibroblast Crosstalk via Paracrine CTGF.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Article
- The role of claudins in homeostasis.Nature reviews. Nephrology · 2023Review
- Digested Cinnamon (International journal of molecular sciences · 2023Article
- Cow Milk Extracellular Vesicle Effects on an In Vitro Model of Intestinal Inflammation.Biomedicines · 2022Article
- Article
- Tumor Necrosis Factor Alpha Effects on the Porcine Intestinal Epithelial Barrier Include Enhanced Expression of TNF Receptor 1.International journal of molecular sciences · 2021Article
- Colon epithelial cell TGFβ signaling modulates the expression of tight junction proteins and barrier function in mice.American journal of physiology. Gastrointestinal and liver physiology · 2021Article
- Corticosteroid enhances epithelial barrier function in intestinal organoids derived from patients with Crohn's disease.Journal of molecular medicine (Berlin, Germany) · 2021Article
- Protective Role of Natural and Semi-Synthetic Tocopherols on TNFα-Induced ROS Production and ICAM-1 and Cl-2 Expression in HT29 Intestinal Epithelial Cells.Antioxidants (Basel, Switzerland) · 2021Article
- Histone H3K9 methylation regulates chronic stress and IL-6-induced colon epithelial permeability and visceral pain.Neurogastroenterology and motility · 2020Article
- Measuring Cell Growth and Junction Development in Epithelial Cells Using Electric Cell-Substrate Impedance Sensing (ECIS).Bio-protocol · 2020Article
- Immunofluorescent Staining of Claudin-2 in Cultured Kidney Tubular Cells.Bio-protocol · 2020Article
- Changes in Radixin Expression and Interaction with Efflux Transporters in the Liver of Adjuvant-Induced Arthritic Rats.Inflammation · 2020Article
- Anti-Obesity Effect ofFrontiers in endocrinology · 2020Article
- Claudin-2: Roles beyond Permeability Functions.International journal of molecular sciences · 2019Review
- Claudin-2 suppresses GEF-H1, RHOA, and MRTF, thereby impacting proliferation and profibrotic phenotype of tubular cells.The Journal of biological chemistry · 2019Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inflammatory cytokine tumor necrosis factor-α (TNF-α) is a pathogenic factor in acute and chronic kidney disease. TNF-α is known to alter expression of epithelial tight junction (TJ) proteins; however, the underlying mechanisms and the impact of this effect on epithelial functions remain poorly defined. Here we describe a novel biphasic effect of TNF-α on TJ protein expression. In LLC-PK1 tubular cells, short-term (1-6 h) TNF-α treatment selectively elevated the expression of the channel-forming TJ protein claudin-2. In contrast, prolonged (>8 h) TNF-α treatment caused a marked downregulation in claudin-2 and an increase in claudin-1, -4, and -7. The early increase and the late decrease in claudin-2 expression involved distinct mechanisms. TNF-α slowed claudin-2 degradation through ERK, causing the early increase. This increase was also mediated by the EGF receptor and RhoA and Rho kinase. In contrast, prolonged TNF-α treatment reduced claudin-2 mRNA levels and promoter activity independent from these signaling pathways. Electric Cell-substrate Impedance Sensing measurements revealed that TNF-α also exerted a biphasic effect on transepithelial resistance (TER) with an initial decrease and a late increase. Thus there was a good temporal correlation between TNF-α-induced claudin-2 protein and TER changes. Indeed, silencing experiments showed that the late TER increase was at least in part caused by reduced claudin-2 expression. Surprisingly, however, claudin-2 silencing did not prevent the early TER drop. Taken together, the TNF-α-induced changes in claudin-2 levels might contribute to TER changes and could also play a role in newly described functions of claudin-2 such as proliferation regulation.
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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.