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首页> 外文期刊>Environmental Epigenetics >Maternal blood lead concentrations, DNA methylation of MEG3 DMR regulating the DLK1/MEG3 imprinted domain and early growth in a multiethnic cohort
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Maternal blood lead concentrations, DNA methylation of MEG3 DMR regulating the DLK1/MEG3 imprinted domain and early growth in a multiethnic cohort

机译：孕妇血铅浓度，MEG3 DMR调节DLK1 / MEG3印迹结构域的DNA甲基化和多族群的早期生长

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Prenatal exposure to lead (Pb) is known to decrease fetal growth; but its effects on postnatal growth and mechanistic insights linking Pb to growth are not clearly defined. Genomically imprinted genes are powerful regulators of growth and energy utilization, and may be particularly vulnerable to environmental Pb exposure. Because imprinting is established early and maintained via DNA methylation, we hypothesized that prenatal Pb exposure alters DNA methylation of imprinted genes resulting in lower birth weight and rapid growth. Pb was measured by inductively coupled plasma mass spectrometry (ICP-MS) in peripheral blood of 321 women of the Newborn Epigenetic STudy (NEST) obtained at gestation ～12 weeks. Linear and logistic regression models were used to evaluate associations between maternal Pb levels, methylation of differentially methylated regions (DMRs) regulating H19, MEG3 , PEG3 , and PLAGL1 , measured by pyrosequencing, birth weight, and weight-for-height z score gains between birth and age 1 year, ages 1–2 years, and 2–3 years. Children born to women with Pb levels in the upper tertile had higher methylation of the regulatory region of the MEG3 DMR imprinted domain (β?=?1.57, SE?=?0.82, P =?0.06). Pb levels were also associated with lower birth weight (β?=??0.41, SE?=?0.15, P =?0.01) and rapid gains in adiposity (OR?=?12.32, 95% CI?=?1.25–121.30, P =?0.03) by age 2–3 years. These data provide early human evidence for Pb associations with hypermethylation at the MEG3 DMR regulatory region and rapid adiposity gain – a risk factor for childhood obesity and cardiometabolic diseases in adulthood.
机译：众所周知，产前暴露于铅（Pb）会降低胎儿的生长;但它对产后生长的影响以及将铅与生长联系起来的机理见解尚不清楚。基因组印记的基因是生长和能量利用的有力调节剂，并且可能特别容易受到环境铅的暴露。由于烙印是早期建立的并通过DNA甲基化来维持，因此我们假设出生前的铅暴露会改变烙印基因的DNA甲基化，从而降低出生体重并快速生长。通过电感耦合等离子体质谱法（ICP-MS）测定妊娠〜12周时获得的321名新生儿表观遗传研究（NEST）妇女外周血中的Pb。线性和逻辑回归模型用于评估母体铅水平，调节H19，MEG3，PEG3和PLAGL1的甲基化差异区域（DMR）的甲基化之间的关联，并通过焦磷酸测序，出生体重和身高比重之间的z得分增加进行测量出生和年龄1岁，1-2岁和2-3岁。上三分位数中具有Pb水平的女性所生的孩子的MEG3 DMR印迹结构域的调节区域的甲基化程度更高（β= 1.57，SE = 0.82，P = 0.06）。铅水平还与较低的出生体重（β≥0.41，SE≥0.15，P = 0.01）和肥胖迅速增加有关（OR≥12.32，95％CI≥1.25–121.30， P =？0.03），年龄为2-3岁。这些数据提供了早期的人类证据，证明铅与MEG3 DMR调控区的甲基化过度有关，并且快速肥胖-这是儿童肥胖和成年期心脏代谢疾病的危险因素。

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