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Genome-wide DNA methylation analysis in alcohol dependence.

机译：酒精依赖的全基因组DNA甲基化分析。

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Genetic, epigenetic, and environmental factors influence the development of alcohol dependence (AD). Recent studies have shown that DNA methylation markers in peripheral blood may serve as risk markers for AD. Yet a genome-wide epigenomic approach investigating the role of DNA methylation in AD has yet to be performed. We conducted a population-based, case-control study of genome-wide DNA methylation to determine if alterations in gene-specific methylation were associated with AD in a Chinese population. Using the Illumina Infinium Human Methylation27 BeadChip, we assessed gene-specific methylation in over 27?000 CpG sites from DNA isolated from lymphocytes in 63 male AD in-patients and 65 male healthy controls. Using a multi-factorial statistical model, we observed differential methylation between cases and controls at multiple CpG sites with the majority of the methylated CpG sites being hypomethylated. Analyses with the online gene set analysis toolkit WebGestalt revealed that the genes of interest were enriched in multiple biological processes involved in AD development. Gene Ontology function annotation showed that stress, immune response and signal transduction were highly associated with AD. Further analysis by the Kyoto Encyclopedia of Genes and Genomes revealed associations with multiple pathways involved in metabolism through cytochrome P450, cytokine-cytokine receptor interaction and calcium signaling. Associations with canonical pathways previously shown to be involved in AD were also observed, such as dehydrogenases 1A (ADH1A), ADH7, aldehyde dehydrogenases 3B2 (ALDH3B2) and cytochrome P450 2A13. We present evidence that alterations in DNA methylation may be associated with AD, which is consistent with epigenetic theory.
机译：遗传，表观遗传和环境因素影响酒精依赖（AD）的发展。最近的研究表明，外周血中的DNA甲基化标志物可能是AD的危险标志物。尚未进行研究DNA甲基化在AD中的作用的全基因组表观基因组方法。我们进行了一项基于人群的病例对照研究，研究了全基因组DNA甲基化的情况，以确定中国人群中基因特异性甲基化的改变是否与AD相关。我们使用Illumina Infinium人类甲基化27 BeadChip，评估了63位男性AD住院患者和65位男性健康对照者从淋巴细胞中分离的DNA中超过27？000 CpG位点的基因特异性甲基化。使用多因素统计模型，我们在多个CpG位点观察到病例与对照之间的甲基化差异，而大多数甲基化的CpG位点为低甲基化。使用在线基因集分析工具包WebGestalt进行的分析显示，感兴趣的基因在涉及AD发育的多个生物学过程中富集。基因本体论功能注释显示应激，免疫应答和信号转导与AD高度相关。 《京都议定书》的基因和基因组百科全书进一步分析显示，与通过细胞色素P450，细胞因子-细胞因子受体相互作用和钙信号传导参与代谢的多种途径相关。还观察到与先前证明参与AD的规范途径的关联，例如脱氢酶1A（ADH1A），ADH7，醛脱氢酶3B2（ALDH3B2）和细胞色素P450 2A13。我们提供的证据表明DNA甲基化的改变可能与AD相关，这与表观遗传学理论是一致的。

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