The association of FKBP5 gene methylation, adolescents' sex, and depressive symptoms among Chinese adolescents: a nested case-control study.
The association of FKBP5 gene methylation, adolescents' sex, and depressive symptoms among Chinese adolescents: a nested case-control study.
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中国青少年 FKBP5 基因甲基化、青少年性别和抑郁症状的关联：一项巢式病例对照研究
DOI：
10.1186/s12888-022-04392-2
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发表时间：
2022-11-30
期刊：
影响因子：
4.4
通讯作者：
中科院分区：
文献类型：
--
作者：
青少年的抑郁症状是世界各地严重的健康问题。据报道，FK506 结合蛋白 5 (FKBP5) 基因中 DNA 甲基化的改变可以调节应激反应，而应激反应与抑郁症状密切相关。然而，大多数有贡献的研究都是在成年人中进行的，相对较少的研究考虑了不同的社会影响和性别差异对抑郁症状患者 FKBP5 DNA 甲基化的影响。本研究旨在测试青少年中 FKBP5 DNA 甲基化与抑郁症状的关联，并探讨上述关联中可能存在的性别差异。本研究采用巢式病例对照设计，在2019年1月至2019年12月的纵向队列研究中进行。中国广东省10所公立高中69个班级的12至17岁青少年参与了这项研究。将基线和随访时均报告有抑郁症状的持续抑郁症状学生视为病例组，随机选择无抑郁症状的学生作为对照组。我们的研究最终纳入了 87 例病例和 151 例对照。通过MassARRAY平台系统对所选基因进行定量甲基化分析。病例组 FKBP5 CpG 位点的总体 DNA 甲基化趋势低于对照组。与健康对照相比，在调整协变量后，在持续抑郁症状的青少年中观察到 FKBP5-12 CpG 1 的甲基化百分比较低（病例：0.94 ± 2.00，对照：0.47 ± 0.92；F = 5.41，P = 0.021），尽管在错误发现率校正后差异的统计显着性消失了（q > 0.05）。此外，在调整社会环境因素后，FKBP5-12 CpG 1 的低甲基化接近显着性（aOR = 0.77；P = 0.055），这表明FKBP5 CpG 位点的低甲基化与持续性抑郁症状之间没有检测到独立关联。此外，在本研究中，我们无法确定 FKBP5 基因甲基化与抑郁症状关联的性别差异。在有持续抑郁症状的青少年中观察到 FKBP5 甲基化水平降低，尽管经过多次测试校正后并不显着。我们在此提出的结果是初步的，强调了与抑郁症状风险相关的复杂的基因-环境相互作用。在线版本包含可在 10.1186/s12888-022-04392-2 获取的补充材料。
Depressive symptoms among adolescents are a serious health concern around the world. Altered DNA methylation in the FK506 binding protein 5 (FKBP5) gene has been reported to regulate stress response, which has been reported to be closely associated with depressive symptoms. However, most of the contributing studies have been conducted among adults and relatively few studies have considered the effect of disparate social influences and sex differences on the DNA methylation of FKBP5 in persons with depressive symptoms. The present study aimed to test the associations of FKBP5 DNA methylation and depressive symptoms among adolescents and explore possible sex differences in the foregoing associations. This study was conducted using a nested case-control design within a longitudinal cohort study from January 2019 to December 2019. Adolescents aged 12 to 17 years from 69 classes in 10 public high schools located in Guangdong province of China participated in this research. Students with persistent depressive symptoms that reported having depressive symptoms at both baseline and follow-up were treated as the case group, and those without depressive symptoms were randomly selected as the control group. Our study finally included 87 cases and 151 controls. Quantitative methylation analyses of the selected gene were carried out by MassARRAY platform System. The overall DNA methylation trend of FKBP5 CpG sites in the case group was lower in comparison to the control group. Compared to healthy controls, lower methylation percentage of FKBP5-12 CpG 1 was observed in adolescents with persistent depressive symptoms after adjusting for covariates (case: 0.94 ± 2.00, control: 0.47 ± 0.92; F = 5.41, P = 0.021), although the statistical significance of the difference was lost after false discovery rate correction (q > 0.05). In addition, the hypomethylation of FKBP5-12 CpG 1 was approaching significance after adjustment for social-environmental factors (aOR = 0.77; P = 0.055), which indicated that no independent association was detected between hypomethylation of FKBP5 CpG sites and persistent depressive symptoms. Furthermore, in the present study, we were unable to identify sex differences in the association of FKBP5 gene methylation with depressive symptoms. The decreased methylation level of FKBP5 was observed in adolescents with persistent depressive symptoms, albeit non-significant after correction for multiple testing. Our results presented here are preliminary and underscore the complex gene-environment interactions relevant to the risk for depressive symptoms. The online version contains supplementary material available at 10.1186/s12888-022-04392-2.
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影响因子：
6.8
作者：
Humphreys, Kathryn L.;Moore, Sarah R.;Gotlib, Ian H.
通讯作者：
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影响因子：
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DOI：
10.1126/stke.2252004re5
发表时间：
2004-03-16
期刊：
Science's STKE : signal transduction knowledge environment
影响因子：
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通讯作者：
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影响因子：
3.7
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通讯作者：
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