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首页> 外文期刊>Progress in Neuro-Psychopharmacology & Biological Psychiatry: An International Research, Review and News Journal >Epigenetic signature of panic disorder: A role of glutamate decarboxylase 1 (GAD1) DNA hypomethylation?
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Epigenetic signature of panic disorder: A role of glutamate decarboxylase 1 (GAD1) DNA hypomethylation?

机译：惊恐症的表观遗传学特征：谷氨酸脱羧酶1（GAD1）DNA低甲基化的作用？

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摘要

Glutamate decarboxylases (GAD67/65; GAD1/. GAD2) are crucially involved in gamma-aminobutyric acid (GABA) synthesis and thus were repeatedly suggested to play an important role in the pathogenesis of anxiety disorders. In the present study, DNA methylation patterns in the GAD1 and GAD2 promoter and GAD1 intron 2 regions were investigated for association with panic disorder, with particular attention to possible effects of environmental factors.Sixty-five patients with panic disorder (f=44, m=21) and 65 matched healthy controls were analyzed for DNA methylation status at 38 GAD1 promoter/intron2 and 10 GAD2 promoter CpG sites via direct sequencing of sodium bisulfate treated DNA extracted from blood cells. Recent positive and negative life events were ascertained. Patients and controls were genotyped for GAD1 rs3762556, rs3791878 and rs3762555, all of which are located in the analyzed promoter region.Patients with panic disorder exhibited significantly lower average GAD1 methylation than healthy controls (p. <. 0.001), particularly at three CpG sites in the promoter as well as in intron 2. The occurrence of negative life events was correlated with relatively decreased average methylation mainly in the female subsample (p=0.01). GAD1 SNP rs3762555 conferred a significantly lower methylation at three GAD1 intron 2 CpG sites (p. <. 0.001). No differential methylation was observed in the GAD2 gene.The present pilot data suggest a potentially compensatory role of GAD1 gene hypomethylation in panic disorder possibly mediating the influence of negative life events and depending on genetic variation. Future studies are warranted to replicate the present finding in independent samples, preferably in a longitudinal design.
机译：谷氨酸脱羧酶（GAD67 / 65; GAD1 /。GAD2）至关重要地参与了γ-氨基丁酸（GABA）的合成，因此反复被建议在焦虑症的发病机理中起重要作用。在本研究中，研究了GAD1和GAD2启动子以及GAD1内含子2区的DNA甲基化模式与恐慌症的相关性，特别注意环境因素的可能影响.65名恐慌症患者（f = 44，m通过对从血细胞中提取的硫酸氢钠处理的DNA进行直接测序，对65个匹配的健康对照进行了38个GAD1启动子/内含子2和10个GAD2启动子CpG位点的DNA甲基化状态分析。确定了最近的积极和消极生活事件。对患者和对照进行GAD1 rs3762556，rs3791878和rs3762555的基因分型，所有这些均位于分析的启动子区域。惊恐障碍患者的GAD1甲基化水平显着低于健康对照组（p。<。0.001），特别是在三个CpG位点在启动子和内含子2中，负性生活事件的发生与平均甲基化相对降低有关，主要在女性子样本中（p = 0.01）。 GAD1 SNP rs3762555在三个GAD1内含子2 CpG位点赋予显着较低的甲基化（p。<。0.001）。在GAD2基因中未观察到差异甲基化。目前的试验数据表明，GAD1基因低甲基化在恐慌症中具有潜在的补偿作用，可能介导负面生活事件的影响并取决于遗传变异。保证未来的研究可以在独立的样本中（最好是在纵向设计中）复制当前发现。

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