Methylation changes at NR3C1 in newborns associate with maternal prenatal stress exposure and newborn birth weight.
Methylation changes at NR3C1 in newborns associate with maternal prenatal stress exposure and newborn birth weight.
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DOI：
10.4161/epi.21180
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发表时间：
2012-08
期刊：
影响因子：
3.7
通讯作者：
Hughes DA
中科院分区：
文献类型：
--
作者：
Mulligan CJ;D'Errico NC;Stees J;Hughes DA
早期的生活经历，包括那些在子宫中的经历，被认为与成人发病的慢性病风险增加有关。基本的假设是，在子宫内有一个发育可塑性的关键期，当选择最适合宫内环境的胎儿表型时。目前的研究首次测试了在刚果民主共和国观察到的极端母亲心理社会应激源可能会改变新生儿的特定基因位点表观遗传标记，从而导致健康结果改变的想法。在这里，我们显示了母亲产前应激、新生儿出生体重和糖皮质激素受体NR3C1启动子中的新生儿甲基化之间的显著相关性。甲基化增加可能会限制后续基因表达的可塑性，并限制受影响个体可能的应激适应反应范围，从而增加他们患成人疾病的风险。
Early life experiences, including those in utero, have been linked to increased risk for adult-onset chronic disease. The underlying assumption is that there is a critical period of developmental plasticity in utero when selection of the fetal phenotype that is best adapted to the intrauterine environment occurs. The current study is the first to test the idea that extreme maternal psychosocial stressors, as observed in the Democratic Republic of Congo, may modify locus-specific epigenetic marks in the newborn resulting in altered health outcomes. Here we show a significant correlation between culturally relevant measures of maternal prenatal stress, newborn birth weight and newborn methylation in the promoter of the glucocorticoid receptor NR3C1. Increased methylation may constrain plasticity in subsequent gene expression and restrict the range of stress adaptation responses possible in affected individuals, thus increasing their risk for adult-onset diseases.