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焦虑症相关 Asb1 启动子中 CpG 甲基化增加:通过流行病学和临床研究及小鼠模型得到的转化研究证据。

Anxiety Associated Increased CpG Methylation in the Promoter of Asb1: A Translational Approach Evidenced by Epidemiological and Clinical Studies and a Murine Model.

机构信息

Institute of Epidemiology II, Helmholtz Zentrum München-German Research Centre for Environmental Health, Neuherberg, Germany.

The Dartmouth Institute for Health Policy and Clinical Practice, Geisel School of Medicine at Dartmouth, Lebanon, NH, USA.

出版信息

Neuropsychopharmacology. 2018 Jan;43(2):342-353. doi: 10.1038/npp.2017.102. Epub 2017 May 25.

Abstract

Epigenetic regulation in anxiety is suggested, but evidence from large studies is needed. We conducted an epigenome-wide association study (EWAS) on anxiety in a population-based cohort and validated our finding in a clinical cohort as well as a murine model. In the KORA cohort, participants (n=1522, age 32-72 years) were administered the Generalized Anxiety Disorder (GAD-7) instrument, whole blood DNA methylation was measured (Illumina 450K BeadChip), and circulating levels of hs-CRP and IL-18 were assessed in the association between anxiety and methylation. DNA methylation was measured using the same instrument in a study of patients with anxiety disorders recruited at the Max Planck Institute of Psychiatry (MPIP, 131 non-medicated cases and 169 controls). To expand our mechanistic understanding, these findings were reverse translated in a mouse model of acute social defeat stress. In the KORA study, participants were classified according to mild, moderate, or severe levels of anxiety (29.4%/6.0%/1.5%, respectively). Severe anxiety was associated with 48.5% increased methylation at a single CpG site (cg12701571) located in the promoter of the gene encoding Asb1 (β-coefficient=0.56 standard error (SE)=0.10, p (Bonferroni)=0.005), a protein hypothetically involved in regulation of cytokine signaling. An interaction between IL-18 and severe anxiety with methylation of this CpG cite showed a tendency towards significance in the total population (p=0.083) and a significant interaction among women (p=0.014). Methylation of the same CpG was positively associated with Panic and Agoraphobia scale (PAS) scores (β=0.005, SE=0.002, p=0.021, n=131) among cases in the MPIP study. In a murine model of acute social defeat stress, Asb1 gene expression was significantly upregulated in a tissue-specific manner (p=0.006), which correlated with upregulation of the neuroimmunomodulating cytokine interleukin 1 beta. Our findings suggest epigenetic regulation of the stress-responsive Asb1 gene in anxiety-related phenotypes. Further studies are necessary to elucidate the causal direction of this association and the potential role of Asb1-mediated immune dysregulation in anxiety disorders.

摘要

焦虑的表观遗传调控得到了提示,但仍需要大样本研究的证据。我们在一个基于人群的队列中进行了焦虑的全基因组关联研究(EWAS),并在临床队列和小鼠模型中验证了我们的发现。在 KORA 队列中,对 1522 名参与者(年龄 32-72 岁)进行了广泛性焦虑障碍(GAD-7)量表评估,测量了全血 DNA 甲基化(Illumina 450K BeadChip),并评估了 hs-CRP 和 IL-18 的循环水平与焦虑之间的关系。在马克斯·普朗克精神病学研究所(MPIP)招募的焦虑症患者的研究中,使用相同的仪器测量了 DNA 甲基化(131 名未用药病例和 169 名对照)。为了扩展我们的机制理解,我们在急性社交挫败应激的小鼠模型中对这些发现进行了反向翻译。在 KORA 研究中,根据轻度、中度或重度焦虑水平对参与者进行分类(分别为 29.4%/6.0%/1.5%)。严重焦虑与单个 CpG 位点(cg12701571)的 48.5%甲基化增加相关,该 CpG 位点位于编码 Asb1 的基因启动子中(β系数=0.56 标准误差(SE)=0.10,p(Bonferroni)=0.005),Asb1 蛋白假设参与了细胞因子信号转导的调控。白细胞介素 18 与严重焦虑之间的相互作用以及该 CpG 位点的甲基化在总人口中显示出有统计学意义的趋势(p=0.083),在女性中存在显著的相互作用(p=0.014)。在 MPIP 研究中的病例中,同一 CpG 的甲基化与惊恐和广场恐惧症量表(PAS)评分呈正相关(β=0.005,SE=0.002,p=0.021,n=131)。在急性社交挫败应激的小鼠模型中,Asb1 基因表达以组织特异性方式显著上调(p=0.006),这与神经免疫调节细胞因子白细胞介素 1β的上调相关。我们的研究结果表明,应激反应基因 Asb1 的表观遗传调控与焦虑相关表型有关。需要进一步的研究来阐明这种关联的因果方向以及 Asb1 介导的免疫失调在焦虑障碍中的潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9770/5729551/c8196303f9b2/npp2017102f1.jpg

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