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Methylation changes at NR3C1 in newborns associate with maternal prenatal stress exposure and newborn birth weight

机译:新生儿NR3C1处的甲基化变化与母亲产前应激暴露和新生儿出生体重有关

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摘要

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.
机译:包括子宫内的早期生活经验与成年慢性病风险增加有关。基本假设是,当发生最适合子宫内环境的胎儿表型选择时,子宫内存在发育可塑性的关键时期。当前的研究是第一个检验这样一种观念的研究,即在刚果民主共和国观察到的极端的产妇心理社会压力源可能会改变新生儿中特定于基因座的表观遗传标记,从而导致健康结果改变。在这里,我们显示了糖皮质激素受体NR3C1启动子中母亲产前压力,新生儿出生体重和新生儿甲基化的文化相关措施之间的显着相关性。增加的甲基化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出现的应激适应反应的范围,从而增加其患成人疾病的风险。

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