Cigarette smoking significantly alters sperm DNA methylation patterns
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PROVIDER: PRJNA472486 | ENA |
REPOSITORIES: ENA
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Project description:Numerous health consequences of tobacco smoke exposure have been characterized, and the effects of smoking on traditional measures of male fertility are well described. However, a growing body of data indicates that pre‐conception paternal smoking also confers increased risk for a number of morbidities on offspring. The mechanism for this increased risk has not been elucidated, but it is likely mediated, at least in part, through epigenetic modifications transmitted through spermatozoa. In this study, we investigated the impact of cigarette smoke exposure on sperm DNA methylation patterns in 78 men who smoke and 78 never‐smokers using the Infinium Human Methylation 450 beadchip. We investigated two models of DNA methylation alterations: (i) consistently altered methylation at specific CpGs or within specific genomic regions and (ii) stochastic DNA methylation alterations manifest as increased variability in genome‐wide methylation patterns in men who smoke. We identified 141 significantly differentially methylated CpGs associated with smoking. In addition, we identified a trend toward increased variance in methylation patterns genome‐wide in sperm DNA from men who smoke compared with never‐smokers. These findings of widespread DNA methylation alterations are consistent with the broad range of offspring heath disparities associated with pre‐conception paternal smoke exposure and warrant further investigation to identify the specific mechanism by which sperm DNA methylation perturbation confers risk to offspring health and whether these changes can be transmitted to offspring and transgenerationally.
2018-05-23 | GSE114753 | GEO
Project description:Numerous health consequences of tobacco smoke exposure have been characterized, and the effects of smoking on traditional measures of male fertility are well described. However, a growing body of data indicates that pre-conception paternal smoking also confers increased risk for a number of morbidities on offspring. The mechanism for this increased risk has not been elucidated, but it is likely mediated, at least in part, through epigenetic modifications transmitted through spermatozoa. In this study, we investigated the impact of cigarette smoke exposure on sperm DNA methylation patterns in 78 men who smoke and 78 never-smokers using the Infinium Human Methylation 450 beadchip. We investigated two models of DNA methylation alterations: (i) consistently altered methylation at specific CpGs or within specific genomic regions and (ii) stochastic DNA methylation alterations manifest as increased variability in genome-wide methylation patterns in men who smoke. We identified 141 significantly differentially methylated CpGs associated with smoking. In addition, we identified a trend toward increased variance in methylation patterns genome-wide in sperm DNA from men who smoke compared with never-smokers. These findings of widespread DNA methylation alterations are consistent with the broad range of offspring heath disparities associated with pre-conception paternal smoke exposure and warrant further investigation to identify the specific mechanism by which sperm DNA methylation perturbation confers risk to offspring health and whether these changes can be transmitted to offspring and transgenerationally.
| S-EPMC5679018 | biostudies-literature
Project description:Transcriptomic analysis of the effects of cigarette smoking on the gene expression in blood in humans
2012-10-01 | GSE23323 | GEO
Project description:Analysis of different expression of microRNAs in immortalized human pancreatic duct epithelial cells treated with cigarette smoke condensate. Cigarette smoking plays vital role in tumorigenesis and development of pancreatic ductal adenocarcinoma. Results provide insight in the machenisms involved in PDAC initiation and progression.
2019-03-24 | GSE103994 | GEO
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:Background. Traditional combustion cigarette (TCC) smoking is an established risk factor for several types of cancer and cardiovascular diseases. Circulating microRNAs (miRNAs) represent key molecules mediating pathogenetic mechanisms, and potential biomarkers for personalized risk assessment. Several transcriptomics studies have showed that TCC smoking globally changes the profile of circulating miRNAs. The use of heat-not-burn cigarettes (HNBCs) as alternative smoking devices is rising exponentially worldwide, with still unknown long-term effects on health. Comprehensive data on the circulating miRNA profile in chronic HNBC smokers are still lacking. Purpose. We aimed at defining the profile of circulating miRNAs in serum samples of chronic exclusive HNBC smokers, and identifying potentially pathogenetic circulating miRNA signatures. Results. Differential expression analysis revealed 101 miRNAs significantly modulated between groups (adjusted p<0.05), with a prevalence of circulating miRNA downregulation in smokers (only 20 miRNAs were upregulated in both groups of smokers). Head-to-head comparison revealed that 65 miRNAs were exclusively modulated in TCC, 26 miRNAs were commonly modulated in both smoker groups, and 10 miRNAs were exclusively modulated in HNBC samples, all versus NS. KEGG pathway analysis performed on target genes of the commonly modulated miRNAs returned cancer-associated and cardiovascular disease pathways. The application of stringent abundance and fold-change criteria to this list nailed down our functional bioinformatic analyses to a network where miR-25-3p and miR-221-3p are main hubs for cardiovascular- and cancer- related molecular pathways, respectively. Conclusions. Our results define for the first time a global miRNA profile in the serum of exclusive chronic HNBC smokers. Despite the globally lower extent of the differences observed, our data suggest a significant detrimental impact of HNBCs on circulating miRNAs.
2023-06-13 | GSE233237 | GEO
Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 2 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed cohousing experiments to test if Paneth cell phenotype is horizontally transmissible as is microbiota. Atg16l1 T300A and littermate controls that were exposed to cigarette smoking were used as microbiota donors, and these donor mice were exposed to smoking for 2 weeks prior to cohousing. Separate groups of Atg16l1 T300A and littermate controls that were not exposed to cigarette smoking were used as microbiota recipients. The microbiota recipients were co-housed with microbiota donors of the same genotype for 4 weeks, during this period the donors continued to be exposed to cigarette smoking. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. At the end of the experiment, the fecal microbiota composition was analyzed by 16S rRNA sequencing.
2018-10-31 | E-MTAB-5720 | biostudies-arrayexpress
Project description:Cigarette smoking accounts for approximately one in five deaths in the United States. Previous genomic studies have primarily focused on gene level differential expression to identify related molecular signatures and pathways, but the genome-wide effects of smoking on alternative isoform regulation and posttranscriptional modulation have not yet been described. We attempted to fill this void by identifying smoking-associated isoform switches and their responsible splicing events and consequences using RNA-seq.
2021-12-01 | GSE171730 | GEO
Project description:Transcriptomic analysis of the effects of cigarette smoking on the gene expression in blood in humans Analysis of gene expression in blood from 22 smokers and 22 non-smokers
2012-10-01 | E-GEOD-23323 | biostudies-arrayexpress
Project description:Introduction Epidemiological studies have shown that smoking is associated with increased incidence of severe viral infections leading to hospitalisation. Moreover, studies in experimental models have identified impaired antiviral responses and altered inflammatory responses, yet it is unclear which immune cells are involved and whether this varies over the course of infection. Methods To test how cigarette smoking affects the response to influenza viral infection over time, female BALB/c mice were exposed to cigarette smoke or air twice a day for 24-28 days and infected with H3N2 influenza or mock infection on day 21. Three and seven days after infection, changes in immune cell populations, and mRNA expression/viral clearance in lung tissue were analysed. Results Smoke-exposed mice lost significantly more weight than air-exposed controls after influenza infection, indicating that smoking resulted in more severe disease. Immune cell and lung tissue transcriptome analysis revealed that neutrophil infiltration was prolonged and macrophage activation dysregulated after infection in smoke-exposed mice compared to air-exposed controls. Expression of genes in IL-6 and interferon pathways was similarly longer active. In parallel, we observed lower clearance of viral RNA in smoke-exposed mice after infection compared to air-exposed controls, indicating ineffective antiviral responses. Adaptive immune responses were unchanged in infected smoking animals compared to nonsmoking mice. Conclusion Altogether, the data from our mouse model indicate that cigarette smoke exposure prolongs innate immune responses against influenza. The results from this study help to explain the susceptibility of current smokers to severe influenza disease.
2024-06-21 | GSE269227 | GEO