ArticleInternational journal of molecular sciences2017
Inhibition of Autophagic Degradation Process Contributes to Claudin-2 Expression Increase and Epithelial Tight Junction Dysfunction in TNF-α Treated Cell Monolayers.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 71 citations in OpenAlex.
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- Therapeutic Potential of Ruberythric Acid in Intestinal Inflammation and Barrier Function Reduction.Preventive nutrition and food science · 2026Article
- Development of a tissue-based risk prediction model combining histology and barrier biomarkers for clinical relapse in ulcerative colitis with endoscopic healing.Therapeutic advances in gastroenterology · 2026Article
- Xanthan gum intake modifies the colon microbiota profile and causes mild colon inflammation in rats.PloS one · 2026Article
- Dysregulated programmed cell death of intestinal epithelial cells in ulcerative colitis: Molecular mechanisms and novel therapeutic interventions (Review).International journal of molecular medicine · 2025Review
- Main genetic factors associated with inflammatory bowel diseases and their consequences on intestinal permeability: involvement in gut inflammation.Journal of gastroenterology · 2025Review
- The Anti-Inflammatory, Immunomodulatory, and Pro-Autophagy Activities of Probiotics for Colorectal Cancer Prevention and Treatment: A Narrative Review.Biomedicines · 2025Review
- Advances in Autophagy-Lysosomal Pathway and Neurodegeneration via Brain-Gut Axis.Biomedicines · 2025Review
- Ghrelin improves small intestinal barrier damage in sepsis by promoting miR-143/ATG2B-mediated autophagy.PloS one · 2025Article
- T1/T2 Proportional Magnetic Resonance Nanoprobe Monitoring Tumor Autophagy during Chemotherapy.Nanomaterials (Basel, Switzerland) · 2024Article
- Dihydroartemisinin Modulates Enteric Glial Cell Heterogeneity to Alleviate Colitis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Harnessing autophagy: A potential breakthrough in digestive disease treatment.World journal of gastroenterology · 2024Article
- Effect of tofacitinib on the phenotype and activity of Caco‑2 cells in a model of inflammatory bowel disease.Experimental and therapeutic medicine · 2024Article
- Intestinal microbiota regulates the gut-thyroid axis: the new dawn of improving Hashimoto thyroiditis.Clinical and experimental medicine · 2024Review
- Article
- The functional antagonist of sphingosine-1-phosphate, FTY720, impairs gut barrier function.Frontiers in pharmacology · 2024Article
- The interaction between autophagy, Helicobacter pylori, and gut microbiota in gastric carcinogenesis.Trends in microbiology · 2023Review
- Digested Cinnamon (International journal of molecular sciences · 2023Article
- Electroacupuncture repairs intestinal barrier by upregulating CB1 through gut microbiota in DSS-induced acute colitis.Chinese medicine · 2023Article
- Fermentation Supernatant of Elderly Feces with Inulin and Partially Hydrolyzed Guar Gum Maintains the Barrier of Inflammation-Induced Caco-2/HT29-MTX-E12 Co-Cultured Cells.Journal of agricultural and food chemistry · 2023Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tight junction dysfunction plays a vital role in some chronic inflammatory diseases. Pro-inflammatory cytokines, especially tumor necrosis factor alpha (TNF-α), act as important factors in intestinal epithelial tight junction dysfunction during inflammatory conditions. Autophagy has also been shown to be crucial in tight junction function and claudin-2 expression, but whether autophagy has an effect on the change of claudin-2 expression and tight junction function induced by TNF-α is still unknown. To answer this question, we examined the expression of claudin-2 protein, transepithelial electrical resistance (TER), and permeability of cell monolayers, autophagy flux change, and lysosomal pH after TNF-α with or without PP242 treatment. Our study showed that claudin-2 expression, intestinal permeability, microtubule-associated protein 1 light chain 3B II (LC3B-II) and sequestosome 1 (P62) expression largely increased while TER values decreased in TNF-α treated cell monolayers. Further research using 3-methyladenine (3-MA), bafilomycin A1, and ad-mCherry-GFP-LC3B adenovirus demonstrated that LC3B-II increase induced by TNF-α was attributed to the inhibition of autophagic degradation. Moreover, both qualitative and quantitative method confirmed the increase of lysosomal pH, and mammalian target of rapamycin (mTOR) inhibitor PP242 treatment relieved this elevation. Moreover, PP242 treatment also alleviated the change of autophagy flux, TER, and claudin-2 expression induced by TNF-α. Therefore, we conclude that increase of claudin-2 levels and intestinal epithelial tight junction dysfunction are partly caused by the inhibition of autophagic degradation in TNF-α treated cell monolayers.
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