ArticleAmerican journal of respiratory cell and molecular biology2008
Distal airways in mice exposed to cigarette smoke: Nrf2-regulated genes are increased in Clara cells.
Article in American journal of respiratory cell and molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 67 citations in OpenAlex.
- Protective factors against oxidative stress in COPD: focus on Nrf2-dependent antioxidant gene expression.Frontiers in medicine · 2025Review
- Club Cells-A Guardian against Occupational Hazards.Biomedicines · 2023Review
- Salivary oxidative stress level among tobacco chewers and smokers: A comparative Study.Journal of advanced pharmaceutical technology & research · 2022Article
- LncRNA Nqo1-AS1 Attenuates Cigarette Smoke-Induced Oxidative Stress by Upregulating its Natural Antisense Transcript Nqo1.Frontiers in pharmacology · 2021Article
- Proteomic Analysis of Vocal Fold Fibroblasts Exposed to Cigarette Smoke Extract: Exploring the Pathophysiology of Reinke's Edema.Molecular & cellular proteomics : MCP · 2019Article
- Assessment of a Highly Multiplexed RNA Sequencing Platform and Comparison to Existing High-Throughput Gene Expression Profiling Techniques.Frontiers in genetics · 2019Article
- [COPD: An early disease].Revue de pneumologie clinique · 2016Review
- Protective role for club cell secretory protein-16 (CC16) in the development of COPD.The European respiratory journal · 2015Article
- Cigarette smoke alters primary human bronchial epithelial cell differentiation at the air-liquid interface.Scientific reports · 2015Article
- Lico A Enhances Nrf2-Mediated Defense Mechanisms against t-BHP-Induced Oxidative Stress and Cell Death via Akt and ERK Activation in RAW 264.7 Cells.Oxidative medicine and cellular longevity · 2015Article
- Linking acute infection to chronic lung disease. The role of IL-33-expressing epithelial progenitor cells.Annals of the American Thoracic Society · 2014Review
- Frataxin deficiency leads to defects in expression of antioxidants and Nrf2 expression in dorsal root ganglia of the Friedreich's ataxia YG8R mouse model.Antioxidants & redox signaling · 2013Article
- Long-term IL-33-producing epithelial progenitor cells in chronic obstructive lung disease.The Journal of clinical investigation · 2013Article
- Effects of side-stream tobacco smoke and smoke extract on glutathione- and oxidative DNA damage repair-deficient mice and blood cells.Mutation research · 2013Article
- Andrographolide protects against cigarette smoke-induced oxidative lung injury via augmentation of Nrf2 activity.British journal of pharmacology · 2013Article
- Article
- Tobacco smoke induced COPD/emphysema in the animal model-are we all on the same page?Frontiers in physiology · 2013Article
- A modular cell-type focused inflammatory process network model for non-diseased pulmonary tissue.Bioinformatics and biology insights · 2013Article
- Gene expression profiling following NRF2 and KEAP1 siRNA knockdown in human lung fibroblasts identifies CCL11/Eotaxin-1 as a novel NRF2 regulated gene.Respiratory research · 2012Article
- Major differences among chemopreventive organoselenocompounds in the sustained elevation of cytoprotective genes.Journal of biochemical and molecular toxicology · 2012Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Cigarette smoke (CS) is the main risk factor for chronic obstructive pulmonary disease (COPD). Terminal bronchioles are critical zones in the pathophysiology of COPD, but little is known about the cellular and molecular changes that occur in cells lining terminal bronchioles in response to CS. We subjected C57BL/6 mice to CS (6 d/wk, up to 6 mo), looked for morphologic changes lining the terminal bronchioles, and used laser capture microdissection to selectively isolate cells in terminal bronchioles to study gene expression. Morphologic and immunohistochemical analyses showed that Clara cell predominance remained despite 6 months of CS exposure. Since Clara cells have a role in protection against oxidative stress, we focused on the expression of antioxidant/detoxification genes using microarray analysis. Of the 35 antioxidant/detoxification genes with at least 2.5-fold increased expression in response to 6 months of CS exposure, 21 were NF-E2-related factor 2 (Nrf2)-regulated genes. Among these were cytochrome P450 1b1, glutathione reductase, thioredoxin reductase, and members of the glutathione S-transferase family, as well as Nrf2 itself. In vitro studies using immortalized murine Clara cells (C22) showed that CS induced the stabilization and nuclear translocation of Nrf2, which correlated with the induction of antioxidant and detoxification genes. Furthermore, decreasing Nrf2 expression by siRNA resulted in a corresponding decrease in CS-induced expression of several antioxidant and detoxification genes by C22 cells. These data suggest that the protective response by Clara cells to CS exposure is predominantly regulated by the transcription factor Nrf2.
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Registered trials
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