ArticleInternational journal of chronic obstructive pulmonary disease2017
MAPK/FoxA2-mediated cigarette smoke-induced squamous metaplasia of bronchial epithelial cells.
Article in International journal of chronic obstructive pulmonary disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Multi-modal evaluation of respiratory diaphragm motion in chronic obstructive pulmonary disease using MRI series and CT images.Japanese journal of radiology · 2024Article
- A Preliminary Study on Transcriptional Regulation of SNP Site C-1888T in the Promoter Region of Human PLUNC Gene and Nasopharyngeal Carcinoma Susceptibility.Genetics research · 2024Article
- Human Airway Basal Cells Undergo Reversible Squamous Differentiation and Reshape Innate Immunity.American journal of respiratory cell and molecular biology · 2023Article
- Article
- Airborne PAHs inhibit gap junctional intercellular communication and activate MAPKs in human bronchial epithelial cell line.Environmental toxicology and pharmacology · 2020Article
- Inactivation of FOXA2 by Respiratory Bacterial Pathogens and Dysregulation of Pulmonary Mucus Homeostasis.Frontiers in immunology · 2020Review
- Cigarette smoke downregulates Nur77 to exacerbate inflammation in chronic obstructive pulmonary disease (COPD).PloS one · 2020Article
- The role of cigarette smoke-induced epigenetic alterations in inflammation.Epigenetics & chromatin · 2019Review
- Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the effect of cigarette smoke (CS) on the development of squamous metaplasia in human airway epithelial cells and the role of MAPK- and FoxA2-signaling pathways in the process. MATERIALS AND
methodsIn an in vitro study, we treated the bronchial epithelial cell line BEAS2B with CS extract, followed by treatment with the ERK inhibitor U0126, the JNK inhibitor SP600125, or the p38 inhibitor SB203580. In vivo, we used a CS-induced rat model. After treatment with CS with or without MAPK inhibitors for 90 days, lung tissues were harvested. p-ERK, p-p38 and p-JNK protein levels in cells and lung tissue were measured using enzyme-linked immunosorbent assays, mRNA- and protein-expression profiles of FoxA2, E-cadherin, CD44, and ZO1 were measured using quantitative real-time polymerase chain reaction and Western blotting, respectively, and morphological changes in bronchial epithelial cells were observed using lung-tissue staining.
resultsIn both the in vitro and in vivo studies, phosphorylation of the ERK1/2, JNK, and p38 proteins was significantly increased (
conclusionMAPK and FoxA2 mediate CS-induced squamous metaplasia. MAPK inhibitors upregulate FoxA2, resulting in a reduction in the degree of squamous metaplasia.
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