ArticleAmerican journal of physiology. Lung cellular and molecular physiology2017
Cigarette smoke disrupts monolayer integrity by altering epithelial cell-cell adhesion and cortical tension.
Article in American journal of physiology. Lung cellular and molecular physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
What it found
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Who cites it
53 citing papers in PubMed, 98 citations in OpenAlex.
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- Epithelial cells in chronic obstructive pulmonary disease exacerbations: Targets for lung repair.Pharmacological reviews · 2026Review
- Epigenetic Dysregulation of the NKX2-1/SPDEF Axis Drives Persistent Goblet Cell Differentiation and Epithelial Barrier Dysfunction in Chronic Obstructive Pulmonary Disease.Respirology (Carlton, Vic.) · 2026Article
- New approaches to uncover COPD pathobiology and develop therapies.JCI insight · 2026Review
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- The Effects of Individual Components of E-Cigarettes on Ion Transport and Airway Surface Liquid Height in Human Bronchial Epithelial Cells.Medicina (Kaunas, Lithuania) · 2025Article
- Novel risk loci encompassing genes influencing STAT3, GPCR, and oxidative stress signaling are associated with co-morbid GERD and COPD.PLoS genetics · 2025Article
- Pathogenic Cell in COPD: Mechanisms of Airway Remodeling, Immune Dysregulation, and Therapeutic Implications.International journal of chronic obstructive pulmonary disease · 2025Review
- Role of E-cadherin in epithelial barrier dysfunction: implications for bacterial infection, inflammation, and disease pathogenesis.Frontiers in cellular and infection microbiology · 2025Review
- Lung Transcriptomics Link Emphysema to Barrier Dysfunction and Macrophage Subpopulations.American journal of respiratory and critical care medicine · 2025Article
- Review
- Microphysiological Models of Lung Epithelium-Alveolar Macrophage Co-Cultures to Study Chronic Lung Disease.Advanced biology · 2024Article
- Thoracic high resolution computed tomography evaluation of imaging abnormalities of 108 lung cancer patients with different pulmonary function.Cancer imaging : the official publication of the International Cancer Imaging Society · 2024Article
- Epigenetic Reprogramming Drives Epithelial Disruption in Chronic Obstructive Pulmonary Disease.American journal of respiratory cell and molecular biology · 2024Article
- Bufei Yishen formula protects the airway epithelial barrier and ameliorates COPD by enhancing autophagy through the Sirt1/AMPK/Foxo3 signaling pathway.Chinese medicine · 2024Article
- Physiological and immunological barriers in the lung.Seminars in immunopathology · 2024Review
- Dysfunctional Epithelial Barrier Is Characterized by Reduced E-Cadherin in Idiopathic Subglottic Stenosis.The Laryngoscope · 2024Article
- Decreased fucosylation impacts epithelial integrity and increases risk for COPD.bioRxiv : the preprint server for biology · 2023Article
- A synthetic coolant (WS-23) in disposable electronic cigarettes impairs cytoskeletal function in EpiAirway microtissues exposed at the air liquid interface.Scientific reports · 2023Article
- Effect of altered human exposome on the skin and mucosal epithelial barrier integrity.Tissue barriers · 2023Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality. Cigarette smoke (CS) drives disease development and progression. The epithelial barrier is damaged by CS with increased monolayer permeability. However, the molecular changes that cause this barrier disruption and the interaction between adhesion proteins and the cytoskeleton are not well defined. We hypothesized that CS alters monolayer integrity by increasing cell contractility and decreasing cell adhesion in epithelia. Normal human airway epithelial cells and primary COPD epithelial cells were exposed to air or CS, and changes measured in protein levels. We measured the cortical tension of individual cells and the stiffness of cells in a monolayer. We confirmed that the changes in acute and subacute in vitro smoke exposure reflect protein changes seen in cell monolayers and tissue sections from COPD patients. Epithelial cells exposed to repetitive CS and those derived from COPD patients have increased monolayer permeability. E-cadherin and β-catenin were reduced in smoke exposed cells as well as in lung tissue sections from patients with COPD. Moreover, repetitive CS caused increased tension in individual cells and cells in a monolayer, which corresponded with increased polymerized actin without changes in myosin IIA and IIB total abundance. Repetitive CS exposure impacts the adhesive intercellular junctions and the tension of epithelial cells by increased actin polymer levels, to further destabilize cell adhesion. Similar changes are seen in epithelial cells from COPD patients indicating that these findings likely contribute to COPD pathology.
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