ArticlePloS one2014
Cigarette smoke extract induces a phenotypic shift in epithelial cells; involvement of HIF1α in mesenchymal transition.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.
- The Association between Smoking and Epiretinal Membrane.Scientific reports · 2016Pooled it
- Chronic Cigarette Smoke Extract Exposure Promotes Genomic and Phenotypic Reprogramming in Lung Cancer Cells.Thoracic cancer · 2026Article
- Hypoxia-inducible factors: Regulatory functions and status as a therapeutic target in gastric cancer (Review).Oncology letters · 2026Review
- Steroids and flavonoids in TRQ ameliorates chronic obstructive pulmonary disease involving Pink1/Parkin-mediated mitophagy.Scientific reports · 2026Article
- Vitronectin regulates lung tissue remodeling and emphysema in chronic obstructive pulmonary disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Review
- Systematic characterization of the components and molecular mechanisms of Jinshui Huanxian granules using UPLC-Orbitrap Fusion MS integrated with network pharmacology.Scientific reports · 2022Article
- Hydrogen Sulfide Inhibits Bronchial Epithelial Cell Epithelial Mesenchymal Transition Through Regulating Endoplasm Reticulum Stress.Frontiers in molecular biosciences · 2022Article
- C-EBPβ mediates in cigarette/IL-17A-induced bronchial epithelial-mesenchymal transition in COPD mice.BMC pulmonary medicine · 2021Article
- Conditioned Media of Adipose-Derived Stem Cells Suppresses Sidestream Cigarette Smoke Extract Induced Cell Death and Epithelial-Mesenchymal Transition in Lung Epithelial Cells.International journal of molecular sciences · 2021Article
- Molecular clock REV-ERBα regulates cigarette smoke-induced pulmonary inflammation and epithelial-mesenchymal transition.JCI insight · 2021Article
- Epiretinal membrane appearance or progression after intravitreal injection in age-related macular degeneration.BMC ophthalmology · 2021Article
- Cigarette Smoke Exposure, Pediatric Lung Disease, and COVID-19.Frontiers in physiology · 2021Review
- Influence of Hypoxia on the Epithelial-Pathogen Interactions in the Lung: Implications for Respiratory Disease.Frontiers in immunology · 2021Review
- Vitamin D Modulates the Response of Bronchial Epithelial Cells Exposed to Cigarette Smoke Extract.Nutrients · 2019Article
- Soluble Wood Smoke Extract Promotes Barrier Dysfunction in Alveolar Epithelial Cells through a MAPK Signaling Pathway.Scientific reports · 2019Article
- Function of cAMP scaffolds in obstructive lung disease: Focus on epithelial-to-mesenchymal transition and oxidative stress.British journal of pharmacology · 2019Review
- Sodium Tanshinone IIA Sulfonate Decreases Cigarette Smoke-Induced Inflammation and Oxidative Stress via Blocking the Activation of MAPK/HIF-1α Signaling Pathway.Frontiers in pharmacology · 2018Article
- βAmerican journal of physiology. Lung cellular and molecular physiology · 2017Article
- Involvement of c-Jun N-Terminal Kinase in TNF-α-Driven Remodeling.American journal of respiratory cell and molecular biology · 2017Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In COPD, matrix remodeling contributes to airflow limitation. Recent evidence suggests that next to fibroblasts, the process of epithelial-mesenchymal transition can contribute to matrix remodeling. CSE has been shown to induce EMT in lung epithelial cells, but the signaling mechanisms involved are largely unknown and subject of this study. EMT was assessed in A549 and BEAS2B cells stimulated with CSE by qPCR, Western blotting and immunofluorescence for epithelial and mesenchymal markers, as were collagen production, cell adhesion and barrier integrity as functional endpoints. Involvement of TGF-β and HIF1α signaling pathways were investigated. In addition, mouse models were used to examine the effects of CS on hypoxia signaling and of hypoxia per se on mesenchymal expression. CSE induced EMT characteristics in A549 and BEAS2B cells, evidenced by decreased expression of epithelial markers and a concomitant increase in mesenchymal marker expression after CSE exposure. Furthermore cells that underwent EMT showed increased production of collagen, decreased adhesion and disrupted barrier integrity. The induction of EMT was found to be independent of TGF-β signaling. On the contrary, CS was able to induce hypoxic signaling in A549 and BEAS2B cells as well as in mice lung tissue. Importantly, HIF1α knock-down prevented induction of mesenchymal markers, increased collagen production and decreased adhesion after CSE exposure, data that are in line with the observed induction of mesenchymal marker expression by hypoxia in vitro and in vivo. Together these data provide evidence that both bronchial and alveolar epithelial cells undergo a functional phenotypic shift in response to CSE exposure which can contribute to increased collagen deposition in COPD lungs. Moreover, HIF1α signaling appears to play an important role in this process.
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Registered trials
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.