Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA94889 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:The goal was to assess global gene expression changes in primary human bronchial epithelial cells exposed to environmental tobacco smoke (ETS) condensate. ETS-C was standardized by HPLC analysis and two timepoints of exposure in two different donor bronchial epithelial cell populations were assessed. These findings demonstrate that even short exposure (4.5 h) to ETS is sufficient to induce a stress response, as reflected by decreased antioxidant levels, induced HSP family members, and modulation of the family of glutathione metabolism enzymes in primary human lung cells. Upon longer exposures (48 h) with ETS-condensate, bronchial epithelial cells arrest at the G2/M phase of the cell cycle. Taken together, these data support a stress-induced state in primary human bronchial epithelial cells that culminates in cell cycle arrest. Keywords: time course, comparative, stress response
2006-12-25 | GSE4234 | GEO
Project description:This SuperSeries is composed of the following subset Series:; GSE14383: Effects of chronic exposure of human bronchial epithelial cells to low doses of cigarette smoke condensate; GSE14385: Response of bronchial epithelial cells to low doses of cigarette smoke condensate and subsequent demethylation agent Experiment Overall Design: Refer to individual Series
2009-08-09 | E-GEOD-14461 | 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:Like tobacco smoking, habitual marijuana smoking causes numerous adverse pulmonary effects. However, the mechanisms of action involved, especially as compared to tobacco smoke, are still unclear. To uncover putative modes of action, this study employed a toxicogenomics approach to compare the toxicological pathways perturbed following exposure to marijuana and tobacco smoke condensate in vitro. Condensates of mainstream smoke from hand-rolled tobacco and marijuana cigarettes were similarly prepared using identical smoking conditions. Murine lung epithelial cells were exposed to low, medium and high concentrations of the smoke condensates for 6 hr. RNA was extracted immediately or after a 4-hr recovery period and hybridized to mouse whole genome microarrays. Tobacco smoke condensate (TSC) exposure was associated with changes in xenobiotic metabolism, oxidative stress, inflammation, and DNA damage response. These same pathways were also significantly affected following marijuana smoke condensate (MSC) exposure. Although the effects of the condensates were largely similar, dose-response analysis indicates that the MSC is substantially more potent than TSC. In addition, steroid biosynthesis, apoptosis, and inflammation pathways were more significantly affected following MSC exposure, whereas m-phase cell cycle pathways were more significantly affected following TSC exposure. MSC exposure also appeared to elicit more severe oxidative stress than TSC exposure, which may account for the greater cytotoxicity of MSC. This study shows that in general, MSC impacts many of the same molecular processes as TSC. However, subtle pathway differences can provide insight into the differential toxicities of the two complex mixtures.
2014-02-06 | GSE44603 | GEO
Project description:Like tobacco smoking, habitual marijuana smoking causes numerous adverse pulmonary effects. However, the mechanisms of action involved, especially as compared to tobacco smoke, are still unclear. To uncover putative modes of action, this study employed a toxicogenomics approach to compare the toxicological pathways perturbed following exposure to marijuana and tobacco smoke condensate in vitro. Condensates of mainstream smoke from hand-rolled tobacco and marijuana cigarettes were similarly prepared using identical smoking conditions. Murine lung epithelial cells were exposed to low, medium and high concentrations of the smoke condensates for 6 hr. RNA was extracted immediately or after a 4-hr recovery period and hybridized to mouse whole genome microarrays. Tobacco smoke condensate (TSC) exposure was associated with changes in xenobiotic metabolism, oxidative stress, inflammation, and DNA damage response. These same pathways were also significantly affected following marijuana smoke condensate (MSC) exposure. Although the effects of the condensates were largely similar, dose-response analysis indicates that the MSC is substantially more potent than TSC. In addition, steroid biosynthesis, apoptosis, and inflammation pathways were more significantly affected following MSC exposure, whereas m-phase cell cycle pathways were more significantly affected following TSC exposure. MSC exposure also appeared to elicit more severe oxidative stress than TSC exposure, which may account for the greater cytotoxicity of MSC. This study shows that in general, MSC impacts many of the same molecular processes as TSC. However, subtle pathway differences can provide insight into the differential toxicities of the two complex mixtures. Murine epithelial lung cells were exposed to tobacco smoke condensates (0, 25, 50, 90 μg/ml) or marijuana smoke condensates (0, 2.5, 5, 10 μg/ml) in serum-free medium for a six hour period. Following the six-hour exposure, cells were either harvested immediately or washed with phosphate-buffered saline and incubated in fresh serum-free medium for a four hour recovery period. Total RNA was extracted from the cells and hybridized against Universal Mouse Reference RNA (Agilent Technologies Canada, Inc.) to Agilent whole mouse genome microarray slides containing 44,000 transcripts. A LOWESS normalization was applied to expression results, and statistically significant genes were identified using the R library MAANOVA. Microarray results were validated by real time RT-PCR.
2014-02-06 | E-GEOD-44603 | biostudies-arrayexpress
Project description:The current study was performed for analysis of the biological effects of vapor from novel tobacco vapor product in comparison with 3R4F cigarette smoke. This study was performed using a three-dimensional culture system composed of an air-liquid interface culture of primary normal human bronchial epithelial cells (MucilAir). The MucilAir tissues were subjected to 17 days of exposure to the aqueous extract of novel tobacco product vapor or 3R4F cigarette smoke. The number of differentially expressed genes increased in MucilAir tissues exposed to aqueous extract of each test product dependent on exposure duration. The number of differentially expressed genes was lower in the tissues exposed to aqueous extract of novel tobacco product vapor compared to the tissues exposed to aqueous extract of 3R4F cigarette smoke.
2020-04-15 | E-MTAB-8920 | biostudies-arrayexpress
Project description:Cigarette smoke (CS) is an aerosol containing more than 6,000 chemicals and one of the risk factor in the development of chronic inflammatory lung disease. To evaluate biological effect of CS on human respiratory tract, organotypic bronchial epithelial cultures can be used to replicate in vivo tissue conditions. The MucilAir organotypic bronchial epithelial cultures were exposed to mainstream aerosols from the 3R4F cigarette and a novel tobacco vapor product (NTV), which we recently developed, using a Vitrocell exposure system. This system consists of three steps: the generation of CS, dilution, and exposure to an air-liquid interface cultured cells in a specially designed module. This exposure scenario mimics CS exposure in the human airway (i.e. direct aerosol exposure to the apical surface of air-liquid interface-cultured cells), We found a dose-dependent increase in the number of differentially expressed genes following 3R4F cigarette smoke exposure, compared with expression in air-exposed controls. In contrast, no changes were detected following exposure to NTV vapor.
2018-02-09 | E-MTAB-6471 | biostudies-arrayexpress
Project description:Analysis of primary human bronchial epithelial cells grown in air liquid interface, exposed in vitro to whole tobacco cigarette smoke (48 puffs, 48 minutes) and electronic cigarette aerosol (400 puffs, 200 minutes). Electronic cigarette exposures included two flavors (menthol, tobacco) both with, and without nicotine.
2016-10-12 | GSE82137 | GEO
Project description:40 current smokers and 40 age- and gender- matched never smokers underwent buccal biopsies.The study had four objectives: (a) to define the effects of smoking on the transcriptome of oral epithelial cells; (b) to determine if any of the effects of tobacco smoke on the transcriptome are gender-dependent; (c) to compare the effects of tobacco smoke exposure on the transcriptome in oral v. bronchial epithelium and (d) to identify agents with the potential to suppress the effects of tobacco smoke on the transcriptome. We used microarrays to provide new insights into the carcinogenic effects of tobacco smoke and offer insights that may prove useful in developing preventive strategies.
2010-02-15 | GSE17913 | GEO