ArticleBMC genomics2018
Transcriptional profiling of human bronchial epithelial cell BEAS-2B exposed to diesel and biomass ultrafine particles.
Article in BMC genomics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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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
31 citing papers in PubMed, 66 citations in OpenAlex.
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- Functional Variant Discovery Identifies a Novel Genetic Link between SPRY2, Wood Smoke, and Asthma.American journal of respiratory cell and molecular biology · 2026Article
- Impact of ethanol as a vehicle for water-insoluble pollutants in BEAS-2B cell toxicity assays.Toxicology mechanisms and methods · 2025Article
- Silica Nanoparticles Induced Epithelial-Mesenchymal Transition in BEAS-2B Cells via ER Stress and SIRT1/HSF1/HSPs Signaling Pathway.Journal of xenobiotics · 2025Article
- Short term effects of changes in air pollutant concentrations during peaks traffic hours on hospitalization for respiratory diseases.Scientific reports · 2025Article
- Pulmonary exposure to renewable diesel exhaust particles alters protein expression and toxicity profiles in bronchoalveolar lavage fluid and plasma of mice.Archives of toxicology · 2025Article
- Occupational exposure and its mechanistic link to allergic asthma and lung function decline; a data-driven approach coupled to mining of adverse outcome pathway signatures.Frontiers in toxicology · 2025Article
- Inhalational exposure history is associated with differential sinonasal gene expression profiles and clinical outcomes in chronic rhinosinusitis patients: A pilot study.International forum of allergy & rhinology · 2024Article
- Association between Airport Ultrafine Particles and Lung Cancer Risk: The Multiethnic Cohort Study.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2024Article
- Diesel exhaust particles alter mitochondrial bioenergetics and cAMP producing capacity in human bronchial epithelial cells.Frontiers in toxicology · 2024Article
- Exposure to urban nanoparticles at low PM[Formula: see text] concentrations as a source of oxidative stress and inflammation.Scientific reports · 2023Article
- The Effects and Pathogenesis of PM2.5 and Its Components on Chronic Obstructive Pulmonary Disease.International journal of chronic obstructive pulmonary disease · 2023Review
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- Emission Factors of COToxics · 2022Article
- Chemical Composition and Toxicity of PMLife (Basel, Switzerland) · 2022Article
- Impact of Air Pollution in Airway Diseases: Role of the Epithelial Cells (Cell Models and Biomarkers).International journal of molecular sciences · 2022Review
- Effect of Angiogenesis and Lymphangiogenesis in Diesel Exhaust Particles Inhalation in Mouse Model of LPS Induced Acute Otitis Media.Frontiers in cellular and infection microbiology · 2022Article
- Deconvolution of multiplexed transcriptional responses to wood smoke particles defines rapid aryl hydrocarbon receptor signaling dynamics.The Journal of biological chemistry · 2021Article
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 3 countries.
Funding
Abstract
backgroundEmissions from diesel vehicles and biomass burning are the principal sources of primary ultrafine particles (UFP). The exposure to UFP has been associated to cardiovascular and pulmonary diseases, including lung cancer. Although many aspects of the toxicology of ambient particulate matter (PM) have been unraveled, the molecular mechanisms activated in human cells by the exposure to UFP are still poorly understood. Here, we present an RNA-seq time-course experiment (five time point after single dose exposure) used to investigate the differential and temporal changes induced in the gene expression of human bronchial epithelial cells (BEAS-2B) by the exposure to UFP generated from diesel and biomass combustion. A combination of different bioinformatics tools (EdgeR, next-maSigPro and reactome FI app-Cytoscape and prioritization strategies) facilitated the analyses the temporal transcriptional pattern, functional gene set enrichment and gene networks related to cellular response to UFP particles.
resultsThe bioinformatics analysis of transcriptional data reveals that the two different UFP induce, since the earliest time points, different transcriptional dynamics resulting in the activation of specific genes. The functional enrichment of differentially expressed genes indicates that the exposure to diesel UFP induces the activation of genes involved in TNFα signaling via NF-kB and inflammatory response, and hypoxia. Conversely, the exposure to ultrafine particles from biomass determines less distinct modifications of the gene expression profiles. Diesel UFP exposure induces the secretion of biomarkers associated to inflammation (CCXL2, EPGN, GREM1, IL1A, IL1B, IL6, IL24, EREG, VEGF) and transcription factors (as NFE2L2, MAFF, HES1, FOSL1, TGIF1) relevant for cardiovascular and lung disease. By means of network reconstruction, four genes (STAT3, HIF1a, NFKB1, KRAS) have emerged as major regulators of transcriptional response of bronchial epithelial cells exposed to diesel exhaust.
conclusionsOverall, this work highlights modifications of the transcriptional landscape in human bronchial cells exposed to UFP and sheds new lights on possible mechanisms by means of which UFP acts as a carcinogen and harmful factor for human health.
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