ArticlePflugers Archiv : European journal of physiology2021
TGF-β1 increases permeability of ciliated airway epithelia via redistribution of claudin 3 from tight junction into cell nuclei.
Article in Pflugers Archiv : European journal of physiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Repression of Connexin26 hemichannel activity protects the barrier function of respiratory airway epithelial cells against LPS-induced alteration.Cell communication and signaling : CCS · 2025Article
- A novel in vitro high-content imaging assay for the prediction of drug-induced lung toxicity.Archives of toxicology · 2024Article
- Canonical and Non-Canonical Localization of Tight Junction Proteins during Early Murine Cranial Development.International journal of molecular sciences · 2024Article
- Claudin-3 facilitates the progression and mediates the tumorigenic effects of TGF-β in glioblastoma multiforme.Medical oncology (Northwood, London, England) · 2023Article
- Midgut microbiota affects the intestinal barrier by producing short-chain fatty acids inFrontiers in microbiology · 2023Article
- Dysfunction of epithelial permeability barrier induced by HMGB1 in 2.5D cultures of human epithelial cells.Tissue barriers · 2022Review
- Serially passaged, conditionally reprogrammed nasal epithelial cells as a model to study epithelial functions and SARS-CoV-2 infection.American journal of physiology. Cell physiology · 2022Article
- Dynamic Python-Based Method Provides Quantitative Analysis of Intercellular Junction Organization DuringFrontiers in cellular and infection microbiology · 2022Article
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
TGF-β1 is a major mediator of airway tissue remodelling during atopic asthma and affects tight junctions (TJs) of airway epithelia. However, its impact on TJs of ciliated epithelia is sparsely investigated. Herein we elaborated effects of TGF-β1 on TJs of primary human bronchial epithelial cells. We demonstrate that TGF-β1 activates TGF-β1 receptors TGFBR1 and TGFBR2 resulting in ALK5-mediated phosphorylation of SMAD2. We observed that TGFBR1 and -R2 localize specifically on motile cilia. TGF-β1 activated accumulation of phosphorylated SMAD2 (pSMAD2-C) at centrioles of motile cilia and at cell nuclei. This triggered an increase in paracellular permeability via cellular redistribution of claudin 3 (CLDN3) from TJs into cell nuclei followed by disruption of epithelial integrity and formation of epithelial lesions. Only ciliated cells express TGF-β1 receptors; however, nuclear accumulations of pSMAD2-C and CLDN3 redistribution were observed with similar time course in ciliated and non-ciliated cells. In summary, we demonstrate a role of motile cilia in TGF-β1 sensing and showed that TGF-β1 disturbs TJ permeability of conductive airway epithelia by redistributing CLDN3 from TJs into cell nuclei. We conclude that the observed effects contribute to loss of epithelial integrity during atopic asthma.
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