a Epidemiology Branch , National Institute of Environmental Health Sciences, National Institutes of Health , Research Triangle Park , NC , USA.
b Epigenetics & Stem Cell Biology Laboratory , National Institute of Environmental Health Sciences, National Institutes of Health , Research Triangle Park , NC , USA.
Epigenetics. 2019 May;14(5):467-476. doi: 10.1080/15592294.2019.1595299. Epub 2019 Mar 28.
Women of advanced maternal age account for an increasing proportion of live births in many developed countries across the globe. Offspring of older mothers are at an increased risk for a variety of subsequent health outcomes, including outcomes that do not manifest until childhood or adulthood. The molecular underpinnings of the association between maternal aging and offspring morbidity remain elusive. However, one possible mechanism is that maternal aging produces specific alterations in the offspring's epigenome in utero, and these epigenetic alterations persist into adulthood. We conducted an epigenome-wide association study (EWAS) of the effect of a mother's age on blood DNA methylation in 2,740 adult daughters using the Illumina Infinium HumanMethylation450 array. A false discovery rate (FDR) q-value threshold of 0.05 was used to identify differentially methylated CpG sites (dmCpGs). We identified 87 dmCpGs associated with increased maternal age. The majority (84%) of the dmCpGs had lower methylation in daughters of older mothers, with an average methylation difference of 0.6% per 5-year increase in mother's age. Thirteen genomic regions contained multiple dmCpGs. Most notably, nine dmCpGs were found in the promoter region of the gene LIM homeobox 8 (LHX8), which plays a pivotal role in female fertility. Other dmCpGs were found in genes associated with metabolically active brown fat, carcinogenesis, and neurodevelopmental disorders. We conclude that maternal age is associated with persistent epigenetic changes in daughters at genes that have intriguing links to health.
高龄产妇在全球许多发达国家的活产儿中所占比例越来越大。大龄母亲的后代患各种后续健康问题的风险增加,包括在儿童期或成年期才出现的健康问题。母龄与后代发病率之间的关联的分子基础仍难以捉摸。然而,一种可能的机制是,母体衰老会导致胎儿在子宫内的表观基因组发生特定改变,并且这些表观遗传改变会持续到成年期。我们使用 Illumina Infinium HumanMethylation450 阵列,对 2740 名成年女儿的血液 DNA 甲基化进行了一项母龄对其影响的全基因组关联研究(EWAS)。使用错误发现率(FDR)q 值阈值 0.05 来识别差异甲基化 CpG 位点(dmCpGs)。我们鉴定出 87 个与母龄增加相关的 dmCpGs。大多数(84%)dmCpGs 在高龄母亲的女儿中呈现出较低的甲基化水平,母亲年龄每增加 5 岁,平均甲基化差异为 0.6%。13 个基因组区域包含多个 dmCpGs。最值得注意的是,在 LIM 同源盒 8 基因(LHX8)的启动子区域发现了 9 个 dmCpGs,该基因在女性生育能力中起着关键作用。其他 dmCpGs 位于与代谢活跃的棕色脂肪、致癌和神经发育障碍相关的基因中。我们的结论是,母龄与女儿基因中的持续表观遗传变化有关,这些基因与健康有有趣的联系。