Effects of chronic exposure of human bronchial epithelial cells to low doses of cigarette smoke condensate
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE14383 | GEO | 2009/08/01
SECONDARY ACCESSION(S): PRJNA114463
REPOSITORIES: GEO
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Project description:BEAS-2B cells have been treated with low doses (20 ug/ml) of CSC for 4 months. As negative control BEAS-2B cells were treated with DMSO (the CSC solvent). Non-treated cells were cultivated in parallel. Experiment Overall Design: After each month total RNA was extracted from three replicates of CSC, DMSO and non-treated BEAS-2B cells and hybridized to Affymetrix GeneChips.
2009-08-09 | E-GEOD-14383 | biostudies-arrayexpress
Project description:The study seeks to identify the epigenetic changes caused by exposure of to cigarette smoke condensate. To this goal human bronchial epithelial cells, BEAS-2B, were treated with 5-aza-2’deoxycitidine and trychostatin A (5AzaC/TSA) subsequent to a chronic exposure (1 month) to cigarette smoke condensate (CSC). As negative control served BEAS-2B cells that were untreated or treated with CSC/DMSO for one month without the subsequent application of 5Aza/TSA. Keywords: stress response
2009-08-01 | GSE14385 | GEO
Project description:The study seeks to identify the epigenetic changes caused by exposure of to cigarette smoke condensate. To this goal human bronchial epithelial cells, BEAS-2B, were treated with 5-aza-2âdeoxycitidine and trychostatin A (5AzaC/TSA) subsequent to a chronic exposure (1 month) to cigarette smoke condensate (CSC). As negative control served BEAS-2B cells that were untreated or treated with CSC/DMSO for one month without the subsequent application of 5Aza/TSA. Experiment Overall Design: BEAS-2B Cells were treated for one month with CSC, DMSO, and left untreated. Subsequently half of the samples were treated with the demethylation agent. So that there were six different conditions with three biological replicates each. One sample had to be excluded because of low quality.
2009-08-15 | E-GEOD-14385 | biostudies-arrayexpress
Project description:Mycbacterium tuberculosis was exposed to cigarette smoke condensate (CSC) in 7H9 dextrose culture media. The transcriptional response to cigarette smoke condensate was compared to that of exposure to the CSC diluent, DMSO..
2021-04-15 | GSE172041 | GEO
Project description:Novel tobacco vapor product, generating vapor without combusting tobacco leaves, has been developed expecting the number and quantity of chemicals in the vapor of these products to be reduced compared to conventional combustible cigarettes. However, if the lower chemical levels correlate with lower toxicity remained to be clarified. Here we examined the difference of conventional cigarette smoke (CS) and novel tobacco vapor product (NTV) using cultured cancer cell line A549 and normal bronchial epithelium cell line BEAS-2B. 0.5% of 3R4F which is conventional CS markedly decreased cell proliferation of both A549 and BEAS-2B, however Ploom TECH or Ploom TECH+ which are commercially available NTV did not affect cell growth. To clarify the cause of decreased cell proliferation, Tunnel assay was performed and clarified that apoptosis was observed in both A549 and BEAS-2B after 24hours after exposure to 3R4F. To further explore the effect of CS to epigenetics, we performed western blotting Histone H2A phosphorylation which is known to correlate transcriptional regulation. Only 3R4F decreased histone H2A phosphorylation of both A549 and BEAS-2B. Then we examined alterations of gene expression after 3R4F treatment of A549 cell. 339, 107, 103 genes which were upregulated more than 2fold were observed in 3R4F, Ploom TECH or Ploom TECH+ treated A549 cell, respectively. Among 339 genes which was upregulated 3R4F, we focused EGR1, FOS, and FOSB gene since they were upregulated more than100 fold. We confirmed this upregulation using RTqPCR. These data suggest that Cigarette smoke but not novel tobacco vapor product cause epigenetic disruption and cell apoptosis possibly by elevating genes such as EGR1.
2020-12-07 | GSE157165 | GEO
Project description:Little is known about alteration of the global gene expression by cigarette smoke (CS) and few biomarkers for smoking-related harm are available. We used Affymetrix HG-U133A GeneChips to measure the transcriptomes in eight cultured lymphocyte samples exposed to cigarette smoke condensate (CSC) in vitro . The in vitro exposure of lymphocytes to CSC significantly changed expression levels of 2,266 genes many of which biologically interacted. They included genes encoding for xenobiotic metabolism and oxidative stress-response (e.g. Nrf2 and AhR signaling pathways), inflammation/immune response (e.g. cytokines), apoptosis, cell cycle and tumorigenesis. However, the magnitude of expression responses for some genes showed high inter-individual variability. Experiment Overall Design: The goals of this study were to evaluate novel gene expression profiles and pathways affected by cigarette smoke condensate (CSC), and to identify potential biomarkers for cigarette smoke exposure and harm. To this end, we isolated the PBMC from eight light smokers, cultured the cells in vitro and exposed them to 2R4F CSC, then determined the gene expression profiles with Affymetrix microarray and analyzed alteration of global gene expression after exposure to CSC.
2009-09-15 | E-GEOD-12586 | biostudies-arrayexpress
Project description:Cigarette smoke (CS)-induced airway inflammation is an important pathologic feature of chronic obstructive pulmonary disease (COPD). Recent studies suggest a potential role of JunD in the regulation of inflammation, but its role in CS-induced airway inflammation has not been reported. This study aimed to determine its role in CS-induced airway inflammation through bioinformatics analysis and in vitro and in vivo experiments. Data from the Gene Expression Omnibus (GEO) database (GSE37147) were analyzed using weighted gene co-expression network analysis (WGCNA) and key driver analysis (KDA), and these analyses were validated using the GSE47460 dataset. The effect of CS on JunD expression was examined in lung tissues of COPD patients and CS-exposed mice and in CS extract (CSE)-exposed BEAS-2B cells. The effects of CSE on airway epithelial inflammatory injury after JunD knockdown or overexpression were also investigated. mRNA-seq and chromatin immunoprecipitation (ChIP)-seq were used to explore the mechanism of JunD-mediated CS-induced airway inflammation. Mice were injected with adeno-associated virus serotype 9 (AAV9)-JunD vector or control vector and then exposed to CS for 4 weeks, and lung tissue morphology and airway inflammation were evaluated. KDA of the lung function-related gene modules in GSE37147 revealed a potential role of JunD in COPD, which was validated in GSE47460. JunD was downregulated in lung tissues of COPD patients and CS-exposed mice and in BEAS-2B cells. JunD knockdown aggravated CSE-induced tumor necrosis factor (TNF)-α and interleukin (IL)-1β release by BEAS-2B cells, while JunD overexpression attenuated these effects. mRNA-seq and ChIP-seq identified several JunD-regulated genes, which are involved in the immune response and TNF signaling pathway and are commonly dysregulated in cell models of airway inflammation. In vivo, JunD overexpression attenuated the CS-induced inflammatory cell infiltration and inflammatory cytokine release in mouse lungs. Thus, JunD is involved in CS-induced airway inflammation and JunD-based therapy may be useful in CS-induced airway disorders.
2020-12-09 | GSE162902 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2009-08-01 | GSE14461 | GEO
Project description:Cigarette smoke is a risk factor for inflammatory diseases, such as atherosclerosis. Tobacco smoke interacts with inflammatory cytokines to produce endothelial dysfunction and induces pro-inflammatory and pro-atherosclerotic effects in vascular tissue. Smooth muscle cells (SMCs) are present in the media of human arteries, and are considered protective against atherosclerotic plaque destabilization. Contractile SMCs are the most prominent cell type in the healthy vessel wall. SMCs are not terminally differentiated, and retain the ability to undergo a phenotypic switch from a contractile to a dedifferentiated synthetic state to express inflammatory markers and a phagocytic activity in response to environmental cues. The aim of our study was to evaluate the effects in human SMCs of lipophilic component from cigarette smoke condensate (CSC) and of hydrophilic components of Electronic-cigarette, Tobacco heating products, or cigarette smoke.
2023-05-10 | PXD041174 | Pride
Project description:Little is known about alteration of the global gene expression by cigarette smoke (CS) and few biomarkers for smoking-related harm are available. We used Affymetrix HG-U133A GeneChips to measure the transcriptomes in eight cultured lymphocyte samples exposed to cigarette smoke condensate (CSC) in vitro . The in vitro exposure of lymphocytes to CSC significantly changed expression levels of 2,266 genes many of which biologically interacted. They included genes encoding for xenobiotic metabolism and oxidative stress-response (e.g. Nrf2 and AhR signaling pathways), inflammation/immune response (e.g. cytokines), apoptosis, cell cycle and tumorigenesis. However, the magnitude of expression responses for some genes showed high inter-individual variability. Keywords: toxic effects on gene expression
2009-08-28 | GSE12586 | GEO