ArticleInhalation toxicology
Altered long non-coding RNAs expression in normal and diseased primary human airway epithelial cells exposed to diesel exhaust particles.
Article in Inhalation toxicology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 1 paper.
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.
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Who cites it
1 citing paper in PubMed.
- Ozonolysis of Terpene Flavor Additives in Vaping Emissions: Elevated Production of Reactive Oxygen Species and Oxidative Stress.Chemical research in toxicology · 2024Article
Corrections and comments
- Erratum issued
Authors and funding
5 authors.
Funding
Abstract
backgroundExposure to diesel exhaust particles (DEP) has been linked to a variety of adverse health effects, including increased morbidity and mortality from cardiovascular diseases, chronic obstructive pulmonary disease (COPD), metabolic syndrome, and lung cancer. The epigenetic changes caused by air pollution have been associated with increased health risks. However, the exact molecular mechanisms underlying the lncRNA-mediated pathogenesis induced by DEP exposure have not been revealed.
methodsThrough RNA-sequencing and integrative analysis of both mRNA and lncRNA profiles, this study investigated the role of lncRNAs in altered gene expression in healthy and diseased human primary epithelial cells (NHBE and DHBE-COPD) exposed to DEP at a dose of 30 μg/cm
resultsWe identified 503 and 563 differentially expressed (DE) mRNAs and a total of 10 and 14 DE lncRNAs in NHBE and DHBE-COPD cells exposed to DEP, respectively. In both NHBE and DHBE-COPD cells, enriched cancer-related pathways were identified at mRNA level, and 3 common lncRNAs
conclusionsOverall, our work highlights the potential importance of lncRNAs in regulating DEP-induced gene expression changes associated with carcinogenesis, and individuals suffering from COPD are likely to be more vulnerable to these environmental triggers.
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