Placental gene networks at the interface between maternal PM(2.5) exposure early in gestation and reduced infant birthweight.

Placental gene networks at the interface between maternal PM(2.5) exposure early in gestation and reduced infant birthweight.
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DOI:
10.1016/j.envres.2021.111342
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发表时间:
2021-08
影响因子:
8.3
通讯作者:
Chen J
Chen J
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Deyssenroth MA;Rosa MJ;Eliot MN;Kelsey KT;Kloog I;Schwartz JD;Wellenius GA;Peng S;Hao K;Marsit CJ;Chen J

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越来越多的证据表明,母亲接触直径 < 2.5 μM 的颗粒物 (PM2.5) 与胎儿生长偏差有关。多项研究表明,胎盘在将母体 PM2.5 暴露对发育中的胎儿的影响传递方面发挥着关键作用。其中包括观察到的空气污染物与候选胎盘特征之间的关联,例如线粒体 DNA 含量、DNA 甲基化和端粒长度。然而,在描述胎盘与空气污染相关健康影响之间的联系途径方面仍然存在差距,包括对孕产妇 PM2.5 暴露影响的胎盘过程的全面分析。在这项研究中,我们检查了胎盘转录组网络的变化与孕前和孕期母亲 PM2.5 暴露以及婴儿出生体重的关系。我们评估了参与罗德岛儿童健康研究 (RIHS) 的研究参与者的 PM2.5 暴露和胎盘 RNA 测序数据。使用结合土地利用回归和卫星遥感数据的混合模型估算每日住宅 PM2.5 水平。采用分布式滞后模型来评估从妊娠前 12 周到出生期间 PM2.5 每周平均值对婴儿出生体重的影响。评估了确定的易感性窗口内的平均 PM2.5 水平与先前使用 WGCNA R 软件包生成的胎盘转录组范围基因共表达网络之间的相关性。我们确定了一个敏感窗口,涵盖妊娠前 12 周和妊娠后 13 周,在此期间,母亲接触 PM2.5 与婴儿出生体重下降显着相关。两个胎盘共表达模块富含涉及氨基酸转运和细胞呼吸的基因,与婴儿出生体重以及在确定的生长限制窗口内平均母亲 PM2.5 暴露水平相关。我们的研究结果表明,母亲接触 PM2.5 可能会改变胎儿生长的胎盘编程,对下游健康影响具有潜在影响,包括对心脏代谢健康结果和病毒感染的易感性。
A growing body of evidence links maternal exposure to particulate matter < 2.5 μM in diameter (PM2.5) and deviations in fetal growth. Several studies suggest that the placenta plays a critical role in conveying the effects of maternal PM2.5 exposure to the developing fetus. These include observed associations between air pollutants and candidate placental features, such as mitochondrial DNA content, DNA methylation and telomere length. However, gaps remain in delineating the pathways linking the placenta to air pollution-related health effects, including a comprehensive profiling of placental processes impacted by maternal PM2.5 exposure. In this study, we examined alterations in a placental transcriptome-wide network in relation to maternal PM2.5 exposure prior to and during pregnancy and infant birthweight. We evaluated PM2.5 exposure and placental RNA-sequencing data among study participants enrolled in the Rhode Island Child Health Study (RICHS). Daily residential PM2.5 levels were estimated using a hybrid model incorporating land-use regression and satellite remote sensing data. Distributed lag models were implemented to assess the impact on infant birthweight due to PM2.5 weekly averages ranging from 12 weeks prior to gestation until birth. Correlations were assessed between PM2.5 levels averaged across the identified window of susceptibility and a placental transcriptome-wide gene coexpression network previously generated using the WGCNA R package. We identified a sensitive window spanning 12 weeks prior to and 13 weeks into gestation during which maternal PM2.5 exposure is significantly associated with reduced infant birthweight. Two placental coexpression modules enriched for genes involved in amino acid transport and cellular respiration were correlated with infant birthweight as well as maternal PM2.5 exposure levels averaged across the identified growth restriction window. Our findings suggest that maternal PM2.5 exposure may alter placental programming of fetal growth, with potential implications for downstream health effects, including susceptibility to cardiometabolic health outcomes and viral infections.
DOI: 10.1016/j.envres.2013.10.008
发表时间: 2014-01-01
影响因子: 8.3
作者:
Basu, Rupa;Harris, Maria;Green, Rochelle
通讯作者: Green, Rochelle
DOI: 10.1186/1471-2431-13-59
发表时间: 2013-04-20
期刊: BMC pediatrics
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发表时间: 2018-06
期刊: Nature reviews. Microbiology
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DOI: 10.1289/ehp.1306837
发表时间: 2014-04
影响因子: 10.4
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DOI: 10.1016/j.envint.2018.08.010
发表时间: 2018-11
影响因子: 11.8
作者:
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通讯作者: Chen J