Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

The kinetics of transcriptomic changes induced by cigarette smoke in rat lungs

ABSTRACT: Gene expression profiling in animal models exposed to cigarette mainstream smoke (CS) shapes up as a promising tool for investigating the molecular mechanisms involved in the onset and development of CS-related disease and may aid in the identification of disease candidate genes. Here we report on differential gene expression in lungs of rats exposed for 2, 7, and 13 weeks to 300 and 600 µg total particulate matter (TPM)/l CS with sacrifice 2, 6, or 20 h after the last exposure. The results showed a distinct, mostly transient, expression pattern of differentially expressed genes encoding antioxidant and xenobiotic-metabolizing enzymes, which confirmed and extended in qualitative and quantitative terms the findings of a former study, where rats were exposed to CS either acutely (once) or short-term (3 weeks). With increasing length of exposure, there was a distinct, mostly sustained, expression of genes implicated in innate and adaptive immune responses, clearly pointing to an emerging inflammatory response. Notably, this inflammatory response included the expression of lung disease-related genes not yet linked to CS exposure, such as osteopontin, arginase 1, and chitinase, as well as genes encoding proteolytic enzymes. Finally, our experiments also revealed a CS exposure-dependent shift in the cyclical expression of genes involved in controlling the circadian rhythm. Altogether, these results provide further insight into the molecular mechanisms of CS-dependent disease onset and development and thus may also be useful for defining CS-specific molecular biomarkers of disease. Keywords: gene expression profiling, cigarette smoke-related disease

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE4644 | GEO | 2006/07/28

SECONDARY ACCESSION(S): PRJNA95279

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

In Utero Cigarette Smoke Affects Allergic Airway Disease But Does Not Alter the Lung Methylome

Project description:Introduction: Prenatal and postnatal cigarette smoke exposure enhances the risk of developing asthma. Despite this as well as other smoking related risks, 11% of women still smoke during pregnancy. We hypothesized that cigarette smoke exposure during prenatal development generates long lasting differential methylation altering transcriptional activity that correlates with disease. Methods: In a house dust mite (HDM) model of allergic airway disease, we measured airway hyperresponsiveness (AHR) and airway inflammation between mice exposed prenatally to cigarette smoke (CS) or filtered air (FA). DNA methylation and gene expression were then measured in lung tissue. Results: We demonstrate that HDM-treated CS mice develop a more severe allergic airway disease compared to HDM-treated FA mice including increased AHR and airway inflammation. While DNA methylation changes between the two HDM-treated groups failed to reach genome-wide significance, 99 DMRs had an uncorrected p-value < 0.001. 6 of these 99 DMRs were selected for validation, based on the immune function of adjacent genes, and only 2 of the 6 DMRs confirmed the bisulfite sequencing data. Additionally, genes near these 6 DMRs (Lif, Il27ra, Tle4, Ptk7, Nfatc2, and Runx3) are differentially expressed between HDM-treated CS mice and HDM-treated FA mice. Conclusions: Our findings confirm that prenatal exposure to cigarette smoke is sufficient to modify allergic airway disease, however, it is unlikely that specific methylation changes account for the exposure-response relationship. These findings highlight the important role in utero cigarette smoke exposure plays in the development of allergic airway disease. Lung DNA methylation profiles of mice exposed in utero to cigarette smoke (CS) then treated with house dust mite (HDM, n = 8) or saline (n = 6), or exposed in utero to filtered air (FA) then treated with HDM (n = 9) or saline (n = 6)

2015-11-19 | E-GEOD-71718 | biostudies-arrayexpress

In Utero Cigarette Smoke Affects Allergic Airway Disease But Does Not Alter the Lung Methylome

2015-11-19 | GSE71718 | GEO

Organotypic human bronchial epithelial cultures (MucilAir) exposed to mainstream aerosols from the 3R4F cigarette and a novel tobacco vapor product

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

Tobacco smoke exposure exacerbates silica-induced pulmonary toxicity in rats

Project description:Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of silicosis. Nevertheless, the precise role of cigarette smoke exposure in silicosis and the underlying mechanisms are not clearly understood. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary response and the underlying mechanisms. Pulmonary toxicity and lung gene expression profiles were determined in male Fischer 344 rats exposed to air, crystalline silica, cigarette smoke or cigarette smoke plus crystalline silica. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by cigarette smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to cigarette smoke, silica or a combination of both compared with the control rats.

2020-11-01 | GSE136945 | GEO

Examining the effects of cigarette smoke on mouse lens through a multi OMIC approach

Project description:Here, we report a multi OMIC (transcriptome, proteome, and metabolome) approach to investigate molecular changes in lens fiber cells (FC) of mice exposed to cigarette smoke (CS). Pregnant mice were placed in a whole-body smoke chamber and a few days later pups were born, which were exposed to CS for 5 hours/day, 5 days/week for a total of 3½ months. We examined the mice exposed to CS for CS-related cataractogenesis after completion of the CS exposure but no cataracts were observed. Lenses of CS-exposed and age-matched, untreated control mice were extracted and lens FC were subjected to multi OMIC profiling. We identified 348 genes, 130 proteins, and 14 metabolites exhibiting significant (p < 0.05) differential levels in lens FC of mice exposed to CS, corresponding to 3.6%, 4.3%, and 5.0% of the total genes, protein, and metabolites, respectively identified in this study. Our multi OMIC approach confirmed that only a small fraction of the transcriptome, the proteome, and the metabolome was perturbed in the lens FC of mice exposed to CS, which suggests that exposure of CS had a minimal effect on the mouse lens. It is worth noting that while our results confirm that CS exposure does not have a substantial impact on the molecular landscape of the mouse lens FC, we cannot rule out that CS exposure for longer durations and/or in combination with other morbidities or environmental factors would have a more robust effect and/or result in cataractogenesis.

2024-03-24 | MTBLS207 | MetaboLights

Multi-omics systems toxicology study of mouse lung assessing the effects of aerosols from two heat-not-burn tobacco products and cigarette smoke

Project description:Cigarette smoke (CS) causes adverse health effects and leads to the development of respiratory disease (chronic obstructive pulmonary disease), cardiovascular disease, and cancer. To reduce the risk of smokers developing smoking-related diseases, Philip Morris International is developing modified risk tobacco products (MRTP). Within a systems toxicology study, we conducted an integrative multi-omics analysis to assess the effects of aerosols from two potential MRTPs - the Carbon Heated Tobacco Product (CHTP) 1.2 and the Tobacco Heating System (THS) 1.2 -, compared with cigarette smoke (CS) at matched nicotine concentrations, on the lung of ApoE-/- mice. Mice were exposed for up to six months and molecular exposure effects were measured by mRNA/miRNA transcriptomics, proteomics, metabolomics, and lipidomics. In addition, the impact of cessation (CESS) or switching to CHTP 1.2 (SWITCH) after three months of CS exposure was evaluated. This data set represents the lung metabolomics data obtained after 3 and 6 months of exposure. The 'Animal ID' or 'CAN' represents the unique animal identifier and allows matching of samples across the different data modalities.

2020-04-25 | MTBLS158 | MetaboLights

Comparison analysis of 2 week old C57BL6J lung exposed to 2 weeks of cigarette smoke compared to age-matched controls

Project description:We hypothesize that gene expression in the cigarette smoke (CS) exposed neonatal lung and age-matched controls will be divergent. CS exposed lung will have divergence of immune response genes and structural genes. The lungs of (6) 2 week old neonatal mice exposed to 2 weeks of CS were compared to the lung of (4) 2 week old age-matched control mice. We utilized microarray analysis to examine transcriptional differences between smoke exposed neonatal lung and age-matched controls. Keywords: comparative expression profiling

2008-01-01 | GSE7310 | GEO

Gene expression profiles in lung tissue of rats following exposure to mainstream cigarette smoke

2006-07-28 | GSE4516 | GEO

Chronic rat exposure to cigarette smoke

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

Gene expression profiles in lung tissue of rats following exposure to mainstream cigarette smoke

Project description:Expression data from rats exposed to cigarette smoke (CS) at three concentrations (sham, 300 µgTPM/l and 600 µgTPM/l) for 13 weeks (5d/week; 2hrs/day) after three different recovery times (2hrs, 6hrs and 20hrs after last treatment); lung tissue Keywords: recovery time course and dose dependency Male Sprague-Dawley rats were nose-only-exposed for 13 weeks in total, 5d/week, 2h/day to following concentrations of mainstream cigarette smoke from the standard reference cigarette 2R4F: sham, 300 µgTPM (Total particulate matter)/l or 600 µgTPM/l.

2006-07-27 | E-GEOD-4516 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data