ArticleRespiratory research2009
Characterisation of the proximal airway squamous metaplasia induced by chronic tobacco smoke exposure in spontaneously hypertensive rats.
Article in Respiratory research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
- Verteporfin, an inhibitor of nuclear YAP, improved multi-ciliated cell differentiation in the airway epithelium.Journal of translational medicine · 2025Article
- Context-dependent roles of mitochondrial LONP1 in orchestrating the balance between airway progenitor versus progeny cells.Cell stem cell · 2024Article
- Animal models and mechanisms of tobacco smoke-induced chronic obstructive pulmonary disease (COPD).Journal of toxicology and environmental health. Part B, Critical reviews · 2023Review
- Lung Regeneration: Cells, Models, and Mechanisms.Cold Spring Harbor perspectives in biology · 2022Review
- Airway basal cells show regionally distinct potential to undergo metaplastic differentiation.eLife · 2022Article
- Differential lung inflammation and injury with tobacco smoke exposure in Wistar Kyoto and spontaneously hypertensive rats.Inhalation toxicology · 2020Article
- Outdoor Air Pollution and New-Onset Airway Disease. An Official American Thoracic Society Workshop Report.Annals of the American Thoracic Society · 2020Article
- Long-Term Sequelae of Smoking and Cessation in Spontaneously Hypertensive Rats.Toxicologic pathology · 2020Article
- Effects of p38MAPK-mediated excision repair cross-complementation 1 expression on prognosis of patients with non-small cell lung cancer.Oncology letters · 2017Article
- In vitro exposure systems and dosimetry assessment tools for inhaled tobacco products: Workshop proceedings, conclusions and paths forward for in vitro model use.Alternatives to laboratory animals : ATLA · 2017Article
- Temporal and Spatial Expression of Transforming Growth Factor-β after Airway Remodeling to Tobacco Smoke in Rats.American journal of respiratory cell and molecular biology · 2016Article
- Similar matrix alterations in alveolar and small airway walls of COPD patients.BMC pulmonary medicine · 2014Article
- IL1RN and KRT13 Expression in Bladder Cancer: Association with Pathologic Characteristics and Smoking Status.Advances in urology · 2014Article
- Comparison of biological responses in rats under various cigarette smoke exposure conditions.Journal of toxicologic pathology · 2013Article
- Use of a soluble epoxide hydrolase inhibitor in smoke-induced chronic obstructive pulmonary disease.American journal of respiratory cell and molecular biology · 2012Article
- Histopathological analogies in chronic pulmonary lesions between cattle and humans: basis for an alternative animal model.TheScientificWorldJournal · 2012Review
- The anti-inflammatory effects of soluble epoxide hydrolase inhibitors are independent of leukocyte recruitment.Biochemical and biophysical research communications · 2011Article
- Review
- Lung injury and cancer: Mechanistic insights into ceramide and EGFR signaling under cigarette smoke.American journal of respiratory cell and molecular biology · 2010Review
- Epipharyngeal Abrasive Therapy Down-regulates the Expression of Cav1.2: A Key Molecule in Influenza Virus Entry.In vivo (Athens, Greece)Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
backgroundContinuous exposure to tobacco smoke (TS) is a key cause of chronic obstructive pulmonary disease (COPD), a complex multifactorial disease that is difficult to model in rodents. The spontaneously hypertensive (SH) rat exhibits several COPD-associated co-morbidities such as hypertension and increased coagulation. We have investigated whether SH rats are a more appropriate animal paradigm of COPD.
methodsSH rats were exposed to TS for 6 hours/day, 3 days/week for 14 weeks, and the lung tissues examined by immunohistochemistry.
resultsTS induced a CK13-positive squamous metaplasia in proximal airways, which also stained for Ki67 and p63. We hypothesise that this lesion arises by basal cell proliferation, which differentiates to a squamous cell phenotype. Differences in staining profiles for the functional markers CC10 and surfactant D, but not phospho-p38, indicated loss of ability to function appropriately as secretory cells. Within the parenchyma, there were also differences in the staining profiles for CC10 and surfactant D, indicating a possible attempt to compensate for losses in proximal airways. In human COPD sections, areas of CK13-positive squamous metaplasia showed sporadic p63 staining, suggesting that unlike the rat, this is not a basal cell-driven lesion.
conclusionThis study demonstrates that although proximal airway metaplasia in rat and human are both CK13+ and therefore squamous, they potentially arise by different mechanisms.
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