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首页> 外文期刊>Environmental Epigenetics >Epigenome-wide association of father’s smoking with offspring DNA methylation: a hypothesis-generating study
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Epigenome-wide association of father’s smoking with offspring DNA methylation: a hypothesis-generating study

机译：父亲吸烟与后代DNA甲基化在表观基因组范围内的联系：一项假说产生的研究

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Epidemiological studies suggest that father’s smoking might influence their future children’s health, but few studies have addressed whether paternal line effects might be related to altered DNA methylation patterns in the offspring. To investigate a potential association between fathers’ smoking exposures and offspring DNA methylation using epigenome-wide association studies. We used data from 195 males and females (11–54?years) participating in two population-based cohorts. DNA methylation was quantified in whole blood using Illumina Infinium MethylationEPIC Beadchip. Comb-p was used to analyse differentially methylated regions (DMRs). Robust multivariate linear models, adjusted for personal/maternal smoking and cell-type proportion, were used to analyse offspring differentially associated probes (DMPs) related to paternal smoking. In sensitivity analyses, we adjusted for socio-economic position and clustering by family. Adjustment for inflation was based on estimation of the empirical null distribution in BACON. Enrichment and pathway analyses were performed on genes annotated to cytosine-phosphate-guanine (CpG) sites using the gometh function in missMethyl. We identified six significant DMRs (Sidak-corrected P values: 0.0006–0.0173), associated with paternal smoking, annotated to genes involved in innate and adaptive immunity, fatty acid synthesis, development and function of neuronal systems and cellular processes. DMP analysis identified 33 CpGs [false discovery rate (FDR) ?0.05]. Following adjustment for genomic control (λ = 1.462), no DMPs remained epigenome-wide significant (FDR??0.05). This hypothesis-generating study found that fathers’ smoking was associated with differential methylation in their adolescent and adult offspring. Future studies are needed to explore the intriguing hypothesis that fathers’ exposures might persistently modify their future offspring’s epigenome.
机译：流行病学研究表明，父亲抽烟可能会影响未来孩子的健康，但很少有研究探讨父系影响是否可能与后代DNA甲基化模式的改变有关。使用表观基因组范围的关联研究来调查父亲的吸烟暴露与后代DNA甲基化之间的潜在关联。我们使用了来自195个男性和女性（11-54岁）的数据，参与了两个基于人口的队列研究。使用Illumina Infinium MethylationEPIC Beadchip对全血中的DNA甲基化进行定量。 Comb-p用于分析差异甲基化区域（DMR）。针对个人/母亲吸烟和细胞类型比例进行调整的稳健多元线性模型用于分析与父亲吸烟有关的后代差异相关探针（DMP）。在敏感性分析中，我们针对社会经济地位和家庭聚类进行了调整。通货膨胀的调整基于对BACON中经验空值分布的估计。使用missMethyl中的gometh功能，对注释到胞嘧啶-磷酸-鸟嘌呤（CpG）位点的基因进行了富集和途径分析。我们鉴定了六个重要的DMR（Sidak校正后的P值：0.0006-0.0173），它们与父亲吸烟有关，并被注释为涉及先天和适应性免疫，脂肪酸合成，神经系统和细胞过程的发育与功能的基因。 DMP分析确定了33 CpGs [错误发现率（FDR）<？0.05]。调整基因组控制后（λ= 1.462），没有DMPs保持在整个表观基因组范围内（FDR <0.05）。这项假设产生的研究发现，父亲的吸烟与青少年和成年后代的甲基化差异有关。需要进行进一步的研究来探索有趣的假设，即父亲的暴露可能会持续改变其未来后代的表观基因组。

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