ArticleChemical research in toxicology2019
Epigenetic Changes in Alveolar Type II Lung Cells of A/J Mice Following Intranasal Treatment with Lipopolysaccharide.
Article in Chemical research in toxicology, 2019. 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, 12 citations in OpenAlex.
- The Bidirectional Relationship Between Diabetes and Cancer: Mechanistic Insights, Epigenetic Intermediaries, and Therapeutic Approaches.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2026Review
- TET1 functions as a tumor suppressor in lung adenocarcinoma through epigenetic remodeling and immune modulation.Epigenetics & chromatin · 2025Article
- Multi-Omics Analysis of the Epigenetic Effects of Inflammation in Murine Type II Pneumocytes.International journal of molecular sciences · 2025Article
- A Multi-Omics Study of Epigenetic Changes in Type II Alveolar Cells of A/J Mice Exposed to Environmental Tobacco Smoke.International journal of molecular sciences · 2024Article
- MiRNAs and Microbiota in Non-Small Cell Lung Cancer (NSCLC): Implications in Pathogenesis and Potential Role in Predicting Response to ICI Treatment.International journal of molecular sciences · 2024Review
- Review
- Multi-Omics Characterization of Inflammatory Bowel Disease-Induced Hyperplasia/Dysplasia in theInternational journal of molecular sciences · 2020Article
- Oral Dosing of Dihydromethysticin Ahead of Tobacco Carcinogen NNK Effectively Prevents Lung Tumorigenesis in A/J Mice.Chemical research in toxicology · 2020Article
- Inhalation exposure to cigarette smoke and inflammatory agents induces epigenetic changes in the lung.Scientific reports · 2020Article
- Pulmonary Micro-Ecological Changes and Potential Microbial Markers in Lung Cancer Patients.Frontiers in oncology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Lipopolysaccharide (LPS) is a bacterial endotoxin present in cigarette smoke. LPS is known to induce inflammation and to increase the size and the multiplicity of lung tumors induced by tobacco-specific nitrosamines. However, the means by which LPS contributes to pulmonary carcinogenesis are not known. One possible mechanism includes LPS-mediated epigenetic deregulation, which leads to aberrant expression of genes involved in DNA repair, tumor suppression, cell cycle progression, and cell growth. In the present work, epigenetic effects of LPS were examined in alveolar type II lung cells of A/J mice. Type II cells were selected because they serve as progenitors of lung adenocarcinomas in smoking induced lung cancer. A/J mice were intranasally treated with LPS, followed by isolation of alveolar type II cells from the lung using cell panning. Global levels of DNA methylation and histone acetylation were quantified by mass spectrometry, while genome-wide transcriptomic changes were characterized by RNA-Seq. LPS treatment was associated with epigenetic changes including decreased cytosine formylation and reduced histone H3K14 and H3K23 acetylation, as well as altered expression levels of genes involved in cell adhesion, inflammation, immune response, and epigenetic regulation. These results suggest that exposure to inflammatory agents in cigarette smoke leads to early epigenetic changes in the lung, which may collaborate with genetic changes to drive the development of lung cancer.
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