Rattus norvegicus
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PROVIDER: PRJNA115657 | ENA |
REPOSITORIES: ENA
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Project description:The kinetics of transcriptomic changes induced by cigarette smoke in rat lungs
| PRJNA95279 | ENA
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
Project description:Although a number of animal model studies have addressed changes in gene expression in the parenchyma and their relationship to emphysema, much less is known about the pathogenesis of cigarette smoke-induced small airway remodeling. In this study we exposed rat tracheal explants to whole smoke for 15 minutes, and then cultured the explants in air. The airway transcriptome was evaluated using RAE 230_2 gene chips. By 2 hours after starting smoke exposure, expression levels of 502 genes were changed up or down by more than 1.5 times (p values <0.01 or less) and by 24 hours 1870 genes were significantly changed up or down. These included genes involved in anti-oxidant protection, epithelial defense and remodeling, inflammatory mediators and transcription factors, and a number of unexpected genes including the MMP-12 inducer, tachykinin-1 (substance P). Pre-treatment of the explants with 1 x 10-7 M dexamethasone reduced the number of significantly changed genes by approximately 47% at 2 hr and 68% at 24 hours and in almost all instances reduced the magnitude of the smoke-induced changes. We conclude that even a very brief exposure to cigarette smoke can lead to rapid changes in the expression of a large number of genes in rat tracheal explants, and that these effects are directly mediated by smoke, without a need for exogenous inflammatory cells. Steroids, contrary to the usual belief, are able to ameliorate many of these changes, at least in this very acute model. Experiment Overall Design: 4x tracheal explants (approx 2-3ug) from each rat (n=6 rats) exposed to control (air), smoke (10 puffs of cigarette smoke, delivered during 15 mins), dexamethasone and dexamethasone + cigarette smoke were used for RNA extraction and hybridization on Rat230_2 Affymetrix microarrays. 1 rat, 4 explants and 4 condiditons. n= 6 rats per group/condition 12 animals = 48 samples total (47 went into analysis because 1 sample failing QC metrics)
2009-04-11 | E-GEOD-15563 | biostudies-arrayexpress
Project description:microRNA expression in rat lung receiving chemopreventive agents and attenuation of cigarette smoke-induced alterations
| PRJNA122317 | ENA
Project description:Airway epithelial cells are the first cells of the lungs to be exposed to the toxic agents contained within cigarette smoke. Accordingly, the response of these cells to this challenge is of considerable interest in the context of diseases in which cigarette smoke is a major aetiological factor. We used Affymetrix microarrays to study the effects of repeated cigarette smoke challenge on three-dimensional human lung airway epithelial cultures.
2011-08-31 | GSE30660 | GEO
Project description:In order to establish a rat embryonic stem cell transcriptome, mRNA from rESC cell line DAc8, the first male germline competent rat ESC line to be described and the first to be used to generate a knockout rat model was characterized using RNA sequencing (RNA-seq) analysis.
2016-09-02 | GSE44150 | GEO
Project description:Airway epithelial cells are the first cells of the lungs to be exposed to the toxic agents contained within cigarette smoke. Accordingly, the response of these cells to this challenge is of considerable interest in the context of diseases in which cigarette smoke is a major aetiological factor. We used Affymetrix microarrays to study the effects of repeated cigarette smoke challenge on three-dimensional human lung airway epithelial cultures. We have used cultures from four individual donors, and compared the effects of repeated cigarette smoke challenge (30mins exposure on four separate days), with no challenge.
2011-08-30 | E-GEOD-30660 | biostudies-arrayexpress
Project description:Although smoking-induced lung disease tends to be more common in the upper lobe, it is not known if this results from the skewed distribution of inhaled cigarette smoke or increased susceptibility of the upper lobes to these disorders. The distribution of inhaled cigarette smoke within the lung is complex, depending on lung pressure-volume relationships, gravity, individual smoking habits and the properties of the individual components of cigarette smoke. With the knowledge that the small airway epithelium is the earliest site of smoking-induced lung disease, and that the small airway epithelium is acutely sensitive to inhaled cigarette smoke with significant changes in the up- and down-regulation of hundreds of genes, we compared upper vs lower lobe gene expression in the small airway epithelium of the same cigarette smokers to determine if the gene expression patterns were similar or different. Active smokers (n=11) with early evidence of smoking-induced lung disease (normal spirometry but low diffusing capacity) underwent bronchoscopy and brushing of the small airway epithelium to compare upper vs lower lobe genome-wide gene expression assessed by microarray. Interestingly, cluster and principal component analysis demonstrated that, for each individual, the expression of the known small airway epithelium smoking-responsive genes were remarkably similar as upper vs lower lobe pairs, although, as expected, there were differences in the smoking-induced changes in gene expression from individual to individual. Thus, while there may be topographic differences in the distribution of cigarette smoke, sufficient smoke reaches the upper vs lower lobe small airway epithelium so that, within each smoker, the upper vs lower lobe gene expression are similar. These observations support the concept that the topographic differences in the occurrence of the smoking-induced lung diseases are likely secondary to topographic differences in the susceptibility of the upper vs lower lobes to cigarette smoke, not the topographic differences in distribution of inhaled cigarette smoke.
2017-03-08 | GSE26307 | GEO
Project description:Synergism of Iraqi Sand/Cigarette Smoke Co-Exposure in Rats
| PRJNA140557 | ENA