In utero cigarette smoke (IUS) exposure, sex differences and disease associations in the developing human fetal lung transcriptome
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE106123 | GEO | 2017/10/25
SECONDARY ACCESSION(S): PRJNA415640
REPOSITORIES: GEO
Similar Datasets
Project description:Whole human fetal lung transcriptome profiles from estimated gestational ages 54 to 137 days post conception. Maternal cigarette smoking status is indicated by cotinine levels measured in the corresponding placenta.
2015-12-22 | GSE68896 | GEO
Project description:Whole human fetal lung transcriptome profiles from estimated gestational ages 54 to 137 days post conception. Maternal cigarette smoking status is indicated by cotinine levels measured in the corresponding placenta. Time series with biological replicates. Whole lung transcriptome profiles, lung development, human fetus, in utero cigarette smoke exposure
2015-12-22 | E-GEOD-68896 | biostudies-arrayexpress
Project description:In the context of male reproductive health, epidemiological studies have observed reduced testis size and abnormal sperm counts and morphology in adult men exposed in utero, although these findings are not always repeated. The ambiguity of these reports is confounded by a lack of controlled animal studies investigating the effects of maternal cigarette smoke exposure on male offspring reproductive health. In this study we examined the effects of cigarette induced reproductive toxicity on male offspring exposed during the gestational and weaning period using our novel direct nasal exposure mouse model of cigarette smoke-induced chronic obstructive pulmonary disease and female subfertility. This was done too gain a better understanding of the adverse effects of gestational maternal smoking on male offspring fertility.
2013-10-23 | GSE51530 | GEO
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:In the context of male reproductive health, epidemiological studies have observed reduced testis size and abnormal sperm counts and morphology in adult men exposed in utero, although these findings are not always repeated. The ambiguity of these reports is confounded by a lack of controlled animal studies investigating the effects of maternal cigarette smoke exposure on male offspring reproductive health. In this study we examined the effects of cigarette induced reproductive toxicity on male offspring exposed during the gestational and weaning period using our novel direct nasal exposure mouse model of cigarette smoke-induced chronic obstructive pulmonary disease and female subfertility. This was done too gain a better understanding of the adverse effects of gestational maternal smoking on male offspring fertility. C57BL/6 5 week-old female mice were exposed via the nose-only to cigarette smoke [twelve 3R4F reference cigarettes (University of Kentucky, USA) twice/day, five times per week, for 12-18 weeks]. Each exposure lasted 60 minutes. Control mice received room air. In total, 27 mice underwent cigarette smoke exposure. Eleven week-old female mice exposed to cigarette smoke for 6 weeks were separated into groups of three and housed with a single control stud male aged 7-8 weeks with proven fertility for a maximum of 12 weeks. Females were monitored every second day for post-coital plugs and pregnancy. Pregnant females were separated into single cages and litter sizes/pup weights recorded. Smoke exposure via dams continued throughout mating/pregnancy/lactation until weaning of pups at 21days post birth. The testis of exposed offspring were then collected for RNA extraction and hybridization on an Illumina Sentrix Mouse ref-8 v2 Beadchip
2013-10-23 | E-GEOD-51530 | biostudies-arrayexpress
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).
2023-05-01 | GSE202215 | 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: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: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.
2015-11-19 | GSE71718 | GEO
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.
2009-09-24 | GSE18235 | GEO