Age, sexual dimorphism and disease associations in the developing human fetal lung transcriptome
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE68896 | GEO | 2015/12/22
SECONDARY ACCESSION(S): PRJNA283988
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. 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:Whole human fetal lung microRNA 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.
2017-10-25 | GSE106123 | GEO
Project description:Paternal exposure to genotoxic compounds is thought to contribute to diseases in their offspring. Therefore, mRNA profiles from sperm in ejaculates of cigarette smokers (N=4) were compared with non-smokers (N=4). Smoking behaviour was verified by assessing cotinine levels in seminal plasma. Gene-expression analysis was subsequently performed using microarray technology (Agilent human 4x44k) to investigate the use of gene-expression profiling as biomarker of gene-environment interactions in human testis
2009-01-28 | GSE13600 | 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.
2013-10-23 | GSE51530 | GEO
Project description:Objectives: To identify transcriptomic differences in the blood and sputum of e-cigarette users compared to conventional cigarettes smokers and healthy controls and describe biological pathways affected by these tobacco products. Methods: Cross-sectional analysis of whole blood and sputum RNA-sequencing data from 8 smokers, 9 e-cigarette users (e-cigs) and 4 controls. Weighted gene co-network analysis (WGCNA) identified gene module associations. Ingenuity Pathway Analysis (IPA) identified canonical pathways associated with tobacco products. Main Results: In blood, a three-group comparison showed 16 differentially expressed genes (DEGs); pair-wise comparison showed 7 DEGs between e-cigs and controls, 35 DEGs between smokers and controls, and 13 DEGs between smokers and e-cigs. In sputum, 438 DEGs were in the three-group comparison. In pair-wise comparisons, there were 2 DEGs between e-cigs and controls, 270 DEGs between smokers and controls, and 468 DEGs between smokers and e-cigs. Only 2 genes in the smokers vs. control comparison overlapped between blood and sputum. Most gene modules identified through WGCNA associated with tobacco product exposures also were associated with cotinine and exhaled CO levels. IPA showed multiple canonical pathways altered by conventional smoking but none by e-cigarette use. Conclusion: Cigarette smoking and e-cigarette use led to transcriptomic changes in both blood and sputum. However, conventional cigarettes induced much stronger transcriptomic responses in both compartments.
2023-05-24 | GSE223736 | GEO
Project description:The Nicotine Metabolic Ratio (NMR), the ratio of two stable metabolites of nicotine, cotinine and trans-3’hydroxycotinin, is a determinant of the number of cigarettes smoked per day (CPD), of smoking topography, responsiveness to treatment via transdermal nicotine for smoking cessation, and carcinogen activation and level. The predominant gene involved in nicotine metabolism is CYP2A6, a highly polymorphic locus located in a cluster of P450 cytochrome protein loci on chr19q13. A recent study comprehensively modeling CYP2A6 genetic variation at seven polymorphisms and a related Nicotine Metabolic Ratio, the cotinine: cotinine+nicotine ratio, explains 72% of NMRC/C+N variation. These results suggest that additional genes may be contributing to nicotine and cotinine metabolism directly or via interaction with CYP2A6 or other genes. To identify additional genes that may influence the NMR, we conducted a genome-wide gene expression analysis of lymphoblastoid cell line (LCL) gene expression in a sample of monozygotic twins discordant for the NMR.
2015-09-30 | GSE51284 | 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:Background: Healthy individuals exposed to low levels of cigarette smoke have a decrement in lung function and higher risk for lung disease compared to unexposed individuals. We hypothesized that healthy individuals exposed to low levels of tobacco smoke must have biologic changes in the small airway epithelium compared to healthy unexposed individuals. Methods: Small airway epithelium was obtained by bronchoscopy from 121 individuals; microarrays assessed genome wide gene expression, and urine nicotine and cotinine were used to categorized subjects as “nonsmokers,” “active smokers,” and “low exposure.” The gene expression data was used to determine the threshold and ID50 of urine nicotine and cotinine at which the small airway epithelium showed abnormal responses. Results: There was no threshold of urine nicotine without an abnormal small airway epithelial response, and only a slightly above detectable threshold abnormal response for cotinine. The nicotine ID50 for nicotine was 25 ng/ml and cotinine 104 ng/ml. Conclusions: The small airway epithelium detects and responds to low levels of tobacco smoke with transcriptome modifications. This provides biologic correlates of epidemiologic studies linking low level tobacco smoke exposure to lung health risk, health, identifies genes in the lung cells most sensitive to tobacco smoke and defines thresholds at the lung epithelium responds to inhaled tobacco smoke. Affymetrix arrays were used to assess the gene expression data of smoking-responsive genes in the in small airway epithelium obtained by fiberoptic bronchoscopy of 48 healthy non-smokers (non-smoker or Nsaets), 65 healthy smokers (smoker), 7 symptomatic smokers (SYMs) and a healthy occasional smoker (OcSs). YSB and LO contributed equally to the study.
2011-02-02 | E-GEOD-19667 | biostudies-arrayexpress
Project description:Cigarette smoking remains the leading cause of preventable death worldwide. Cigarette smoking behaviors (e.g., initiation, nicotine dependence, cessation) are heritable, and many genetic risk loci have been identified. However, the neurobiological mechanisms underlying the genetic risk loci along the trajectory of smoking are largely unknown. RNA-sequencing (RNA-seq) differences between smokers and nonsmokers can provide insight into mechanisms that predispose to smoking behaviors and consequences of the smoking exposure itself. Here, we provide RNA-seq data generated in nucleus accumbens, an addiction-relevant brain tissue, from 223 deceased individuals: 50 current cigarette smokers, 171 nonsmokers, and 2 individuals with undetermined smoking status. DNA methylation data on the Illumina HumanMethylationEPIC array are also available on most of these individuals and made available (GEO accession number GSE147040).
2021-04-14 | GSE171936 | GEO
Project description:Rationale: Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD) and lung cancer remains significantly higher compared to never-smokers. Objectives: Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE), we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. Methods: SAE was collected from 10th to 12th order bronchi using fiberoptic bronchoscopy. Affymetrix miRNA 2.0 arrays were used to assess miRNA expression in the SAE from 10 healthy never-smokers and 10 healthy smokers, before and after they quit for 3 months. Smoking status was determined by urine nicotine and cotinine measurement. Results: There were significant differences in the expression of 34 miRNAs between healthy smokers and healthy never-smokers (p<0.01, fold-change >1.5), with functions associated with lung development, airway epithelium differentiation, inflammation and cancer. After quitting smoking for 3 months, 12 out of the 34 miRNAs did not return to normal levels, with Wnt/β-catenin signaling pathway the top enriched pathway of the target genes of the persistent deregulated miRNAs. Conclusions: In the context that many of these persistent smoking-dependent miRNAs are associated with differentiation, inflammation diseases or lung cancer, it is likely that persistent smoking-related changes in small airway epithelium miRNAs play a role in the subsequent development of these disorders. MicroRNA profiling identified 34 miRNAs up-regulated by cigarette smoking in human small airway epithelium. Even after quitting smoking for 3 months, 12 miRNAs didnât return to normal level.
2015-11-23 | E-GEOD-53519 | biostudies-arrayexpress