Smoking effect on DNA methylation in human blood cell types
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ABSTRACT:
PROVIDER: PRJNA932769 | ENA |
REPOSITORIES: ENA
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Project description:Tobacco smoking alters DNA methylation profiles of immune cells which may underpin some of the pathogenesis of smoking-associated diseases. However, approaches linking smoking-driven epigenetic effects in specific immune cell types with disease risk are limited. We isolated six leukocyte subtypes, CD14+ monocytes, CD15+ granulocytes, CD19+ B cells, CD4+ T cells, CD8+ T cells, and CD56+ natural killer cells, from whole blood of healthy adult smokers and nonsmokers for epigenome-wide association study (EWAS).
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Project description:Smoking effect on DNA methylation in human blood CD8T cells
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Project description:DNA methylation is an epigenetic event whose pattern is altered frequently in a wide variety of human diseases. Smoking affects DNA methylation possibly leading to abnormal expression of a broad spectrum of genes which in turn may result to the various side effects and diseases associated with smoking. The long term effects of smoking have been widely studied but the mechanism(s) by which those effects may be reversible by smoking cessation are not clearly understood. Here, we conducted an epigenome-wide association study in peripheral-blood DNA in 464 individuals who were current, former and never-smokers. We identified 15 distinct loci (10 of which were novel) where DNA methylation was reduced in smokers and was reversed (but did not reach non-smoking levels) upon smoking cessation within 12 weeks. Although the functional impact of this reversal of DNA methylation is still not understood, this study illustrates the potential of epigenomics to provide insights into mechanisms of environmental and lifestyle exposures, and to suggest new avenues for clinical intervention
2014-11-25 | GSE50660 | GEO
Project description:DNA methylation is an epigenetic event whose pattern is altered frequently in a wide variety of human diseases. Smoking affects DNA methylation possibly leading to abnormal expression of a broad spectrum of genes which in turn may result to the various side effects and diseases associated with smoking. The long term effects of smoking have been widely studied but the mechanism(s) by which those effects may be reversible by smoking cessation are not clearly understood. Here, we conducted an epigenome-wide association study in peripheral-blood DNA in 464 individuals who were current, former and never-smokers. We identified 15 distinct loci (10 of which were novel) where DNA methylation was reduced in smokers and was reversed (but did not reach non-smoking levels) upon smoking cessation within 12 weeks. Although the functional impact of this reversal of DNA methylation is still not understood, this study illustrates the potential of epigenomics to provide insights into mechanisms of environmental and lifestyle exposures, and to suggest new avenues for clinical intervention Bisulfite converted DNA from the 464 samples were hybridized to the Illumina Infinium HumanMethylation450 BeadChip
2014-11-25 | E-GEOD-50660 | biostudies-arrayexpress
Project description:Background: Epigenetics is involved in various human diseases. Smoking is one of the most common environmental factors causing epigenetic changes. The DNA methylation changes and mechanisms after quitting smoking have not yet been defined. The present study examined the changes in DNA methylation level before and after short-term smoking cessation and explored the potential mechanism. Methods: Whole blood and clinical data were collected in 8 patients before and after short-term smoking cessation, DNA methylation was assessed, and differentially methylated sites were analyzed, followed by a comprehensive analysis of the differentially methylated sites with clinical data. GO/KEGG enrichment and protein-protein interaction (PPI) network identified the hub genes. The differentially methylated sites were detected by GEO2R between former smoking and current smoking in GSE50660 from the GEO database. Then, a Venn analysis was carried out using the differentially methylated sites. GO/KEGG enrichment analysis was performed on the genes corresponding to the common DNA methylation sites, the PPI network was constructed, and hub genes were predicted. The enriched genes associated with the cell cycle were selected, and the gene expression was analyzed in pan-cancer based on the TCGA database. Results: Most of the DNA methylation levels were decreased after short-term smoking cessation; a total of 694 hypermethylated CPG sites and 3184 hypomethylated CPG sites were identified. The DNA methylation levels altered according to the clinical data (body weight, expiratory, and tobacco dependence score). Enrichment analysis, construction of PPI network, and pan-cancer analysis suggested that smoking cessation may be involved in various biological processes. Conclusions: Smoking cessation leads to epigenetic changes, mainly observed in the decline of most DNA methylation levels. Bioinformatics further identified the biologically relevant changes after short-term smoking cessation.
2023-08-08 | GSE201532 | GEO
Project description:Smoking is common in people who live with HIV infection and has significant adverse effects on HIV outcomes. The impacts of smoking on methylome has been well established in non-HIV populations. However, the smoking’s effects on host methylome in HIV-positive population has not been investigated and it is unknown if smoking-associated DNA methylation link to HIV outcomes. In this study, we applied machine learning methods selected smoking-associated DNA methylation features to predict HIV related frailty and mortality.
2019-07-23 | GSE117860 | GEO
Project description:Smoking is common in people who live with HIV infection and has significant adverse effects on HIV outcomes. The impacts of smoking on methylome has been well established in non-HIV populations. However, the smoking’s effects on host methylome in HIV-positive population has not been investigated and it is unknown if smoking-associated DNA methylation link to HIV outcomes. In this study, we applied machine learning methods selected smoking-associated DNA methylation features to predict HIV related frailty and mortality.
2019-07-23 | GSE117859 | 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.
2018-05-23 | GSE114753 | GEO