| Title | Transcriptional profiling of human bronchial epithelial cell BEAS-2B exposed to diesel and biomass ultrafine particles. |
|---|---|
| Publication Type | Articolo su Rivista peer-reviewed |
| Year of Publication | 2018 |
| Authors | Grilli, Andrea, Bengalli Rossella, Longhin Eleonora, Capasso Laura, Proverbio Maria Carla, Forcato Mattia, Bicciato Silvio, Gualtieri Maurizio, Battaglia Cristina, and Camatini Marina |
| Journal | BMC Genomics |
| Volume | 19 |
| Issue | 1 |
| Pagination | 302 |
| Date Published | 2018 Apr 27 |
| ISSN | 14712164 |
| Keywords | article, BEAS 2B cell line, Biodiesel, bioinformatics, Biomass, Bronchi, bronchus, cardiovascular disease, CCXL2 gene, cell culture, Cells, controlled study, Cultured, cytology, disease association, drug effect, environmental exposure, Epithelial Cells, epithelium cell, EREG gene, exhaust gas, FOSL1 gene, gene, Gene expression, gene expression profiling, gene expression regulation, genetic transcription, GREM1 gene, HBEC cell line (bronchial epithelium), HES1 gene, HIF1a gene, human, human cell, Humans, hypoxia, IL1A gene, IL1B gene, IL24 gene, IL6 gene, inflammation, intoxication, lung disease, MAFF gene, metabolism, NF kappa B gene, NFE2L2 gene, NFKB1 gene, oncogene K ras, particle size, particulate matter, RNA sequence, signal transduction, STAT3 gene, TGIF1 gene, TNF alpha gene, transcriptome, VEGF gene, Vehicle Emissions |
| Abstract | BACKGROUND: Emissions 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. RESULTS: The 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. CONCLUSIONS: Overall, 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. |
| Notes | cited By 4 |
| URL | https://www.scopus.com/inward/record.uri?eid=2-s2.0-85046128179&doi=10.1186%2fs12864-018-4679-9&partnerID=40&md5=1d23d5ae42762dbca6fcbe1fd1d4b922 |
| DOI | 10.1186/s12864-018-4679-9 |
| Alternate Journal | BMC Genomics |
| Citation Key | 6449 |
| PubMed ID | 29703138 |
| PubMed Central ID | PMC5923024 |
| Grant List | 2013-1038 / / Fondazione Cariplo / Epigenetics Flagship project CNR-MIUR / / MIUR / |
