Effect of 10 Cigarette Smoke Condensates on Primary Human Airway Epithelial Cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE18235 | GEO | 2009/09/24
SECONDARY ACCESSION(S): PRJNA119621
REPOSITORIES: GEO
Similar Datasets
Project description:Nine cigarette smoke condensates (CSCs) were produced under a standard ISO smoking machine regimen and one was produced by a more intense smoking machine regimen. These CSCs were used to treat primary normal human bronchial epithelial cells for 18 hours. Experiment Overall Design: Primary human bronchial/tracheal epithelial cells were grown in culture and treated with 10 different sources of cigarette smoke condensates.
2009-10-03 | E-GEOD-18235 | 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. 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:Cigarette smoking is one of the major risk factors for Pancreatic Cancer. Our goal in this study is to investigate mechanistic link between smoking and pancreatic cancer stem cell (CSC) enrichment. We report that cigarette smoking augments pancreatic CSCs and this process occurs by the activation of Paf1/PD2, a major stem ness marker. We also report that the cigarette smoke activates Paf1/PD2 through nACHRα7-ERK1/2-FOSL1 signaling axis.
2018-07-21 | GSE101726 | 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.
2014-02-06 | GSE44603 | GEO
Project description:Chronic obstructive pulmonary disease is a smoking-related disease that lacks effective therapies due partly to the poor understanding of disease pathogenesis. The aim of this study was to identify molecular pathways which could be responsible for the damaging consequences of smoking. To do this, we employed recently described bioinformatic methods to analyze differences in global gene expression, which we then related to the pathological changes induced by cigarette smoke (CS). Sprague-Dawley rats were exposed to whole-body CS for 1 day and for various periods up to 8 months. Keywords: Timecourse
2007-12-11 | GSE7079 | GEO
Project description:A number of studies have shown that cigarette smoking produces a field defect, such that genetic mutations induced by smoking occur throughout the lung and its intra and extra-pulmonary airways. Based on this concept, we have begun this study, which has as its goal the definition of the normal airway transcriptome, an analysis of how that transcriptome is affected by cigarette smoke, and to explore the reversibility of altered gene expression when smoking has been discontinued. We have obtained brushings from intra-pulmonary airways (the right upper lobe carina) and scrapings from the buccal mucosa, from normal smoking and non-smoking volunteers (including 34 Current Smokers, 23 Never Smokers and 18 Former Smokers). RNA was isolated from these samples and gene expression profiles from intra-pulmonary airway epithelial cells were analyzed using Affymetrix U133A human gene expression arrays. All microarray data from the experiments described above have been stored, preprocessed and analyzed in a relational MySQL database that is accessible through our website at http://pulm.bumc.bu.edu/aged Keywords = Lung Keywords = Cancer Keywords = Airway Keywords = Epithelium Keywords = Transcriptome Keywords = Gene Keywords = Microarray Keywords = Bronchi Keywords: repeat sample
2004-01-27 | GSE994 | GEO
Project description:These studies tested the hypotheses that smoke induces changes in mRNA profiles that are dependent on sex and the health status of the lung, and that the effects of smoke are different after 1 day compared to 5 days of smoke exposure. The ways in which the lungs modulate their response to cigarette smoke after repeated exposures are important for understanding the toxicology of smoke, for developing biomarkers of chronic smoke exposure, and for understanding the therapeutic potential in regulatory signaling pathways that are beneficial or detrimental to lung health. Sex-matched 5-7-week old wildtype (WT) and Scnn1b-overexpressing (BENaC) littermates were exposed to cigarette smoke or sham (room air) exposure. Exposure occurred in a plexiglass chamber attached to a smoke delivery device using an exposure chamber and smoking machine (inExpose Exposure System, SCIREQ, Chandler, AZ). Mice were exposed to mainstream + sidestream smoke from 6 reference cigarettes with filters removed per day (3R4F research cigarettes, University of Kentucky). Each cigarette was puffed for 2 sec every 25 sec, using the standard Federal Trade Commission smoking machine protocol. The sham-exposed control mice were exposed to room air in the exposure chamber for a time equivalent to that needed for active smoke exposure. Mice were exposed to cigarette or sham smoke for 1 day or 5 consecutive days. Samples were harvested 4 hours after the completion of the final smoke exposure. The right lung was used for gene expression analysis.
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2016-02-15 | GSE22456 | GEO
Project description:Circular RNAs, once thought to be a result of splicing errors, have been found to be involved in various molecular processes and in pathology of various diseases, including cancer and neurodegenerative disease. Additionally, circRNA expression was found to be altered by lifestyle habits, such as smoking cigarettes. Past studies have revealed that the rate of smoking remains high in the HIV-positive population. In this study, we isolated total RNA from uninfected T-cells that have been exposed to cigarette smoke and compared the expression levels of circRNAs to those of T-cells that were not exposed to cigarette smoke. We identified certain circRNAs that were upregulated or downregulated in T-cells when exposed to cigarette smoke. These data indicate that the study of circRNAs is warranted within the context of HIV infection.
2023-04-05 | GSE228979 | GEO
Project description:Cigarette smoke is a major risk factor for the development and progression of chronic obstructive pulmonary disease. Tobacco smoking is also the main cause of lung cancer and the main preventable cause of other lung and heart disease. Strategies to eliminate cigarette smoking have led to the emergence of new tobacco-related products as alternatives for cigarette smoking or tools for smoking cessation. Electronic cigarettes (E-cigarettes) have been introduced to the market in recent years as an alternative to smoking conventional cigarettes. E-cigarettes are nicotine delivery devices by heating and converting to aerosol a liquid mixture composed of propylene glycol, vegetable glycerine, flavouring chemicals, and nicotine. Despite the lack of appropriate studies, e-cigarettes are nowadays widely used and advertised as safe cigarette replacements and the number of users is rapidly growing. Unlike cigarette smoke, where the determinant effects are well studied and documented, very limited amount of research has been done on the health effects and public health of e-cigarettes. The study aims to investigate the effects of e-cigarette vapour extract on gene expression in different primary isolated mouse lung cells [pulmonary arterial smooth muscle cells (PASMC) and alveolar epithelial type two cells (AECII)]. The cells will be exposed to e-cigarette vapour extract (ECVE).
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