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首页> 外文期刊>Journal of applied toxicology >Bisphenol A affects placental layers morphology and angiogenesis during early pregnancy phase in mice
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Bisphenol A affects placental layers morphology and angiogenesis during early pregnancy phase in mice

机译：双酚A在小鼠早期妊娠期间影响胎盘层形态和血管生成

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Bisphenol A (BPA) is a widespread endocrine disrupter mainly used in food contact plastics. Much evidence supports the adverse effects of BPA, particularly on susceptible groups such as pregnant women. The present study considered placental development - relevant for pregnancy outcomes and fetal nutrition/programming - as a potential target of BPA. Pregnant CD-1 mice were administered per os with vehicle, 0.5 (BPA05) or 50mgkg(-1) (BPA50) body weight day(-1) of BPA, from gestational day (GD) 1 to GD11. At GD12, BPA50 induced significant degeneration and necrosis of giant cells, increased vacuolization in the junctional zone in the absence of glycogen accumulation and reduction of the spongiotrophoblast layer. In addition, BPA05 induced glycogen depletion as well as significant nuclear accumulation of -catenin in trophoblasts of labyrinthine and spongiotrophoblast layers, supporting the activation of the Wnt/-catenin pathway. Transcriptomic analysis indicated that BPA05 promoted and BPA50 inhibited blood vessel development and branching; morphologically, maternal vessels were narrower in BPA05 placentas, whereas embryonic and maternal vessels were irregularly dilated in the labyrinth of BPA50 placentas. Quantitative polymerase chain reaction evidenced an estrogen receptor induction by BPA50, which did not correspond to downstream genes activation; indeed, the transcription factor binding sites analysis supported the AhR/Arnt complex as regulator of BPA50-modulated genes. Conversely, Creb appeared as the main transcription factor regulating BPA05-modulated genes. Embryonic structures (head, forelimb) showed divergent perturbations upon BPA05 or BPA50 exposure, potentially related to unbalanced embryonic nutrition and/or to modulation of genes involved in embryo development. Our findings support placenta as an important target of BPA, even at environmentally relevant dose levels. Copyright (c) 2015 John Wiley & Sons, Ltd.
机译：双酚A（BPA）是一种主要用于食品接触塑料的广泛内分泌失坡。许多证据支持BPA的不利影响，特别是对孕妇等易感群体。本研究考虑了胎盘发展 - 与妊娠结局和胎儿营养/编程相关 - 作为BPA的潜在目标。使用载体，0.5（BPA05）或50mgkg（BPA50）体重（BPA50）体重日（-1）的BPA，从妊娠期（GD）1至GD11，每对孕系，0.5（BPA05）或50mgkg（BPA50）施用妊娠CD-1小鼠。在GD12，BPA50诱导巨细胞的显着变性和坏死，在没有糖原积聚和减少的肾上腺素细胞层的情况下增加了连接区的真空化。此外，BPA05诱导糖原耗尽以及息肉蛋白滋养细胞层中的-Catenin的显着核积累，其支持Wnt / -catenin途径的活化。转录组分析表明BPA05促进和BPA50抑制血管发育和分支;形态学上，母体血管在BPA05胎盘中较窄，而胚胎和母体血管在BPA50胎盘的迷宫中不规则地扩张。定量聚合酶链反应证明了BPA50的雌激素受体诱导，其与下游基因活化不相对应;实际上，转录因子结合位点分析支持AHR / ARNT复合物作为BPA50调制基因的调节剂。相反，CREB出现为调节BPA05调制基因的主要转录因子。胚胎结构（头部，前肢）显示BPA05或BPA50暴露的发散性扰动，潜在地与不平衡的胚胎营养和/或调节胚胎发育中的基因。我们的研究结果支持胎盘作为BPA的重要目标，即使在环境相关的剂量水平。版权所有（c）2015 John Wiley＆Sons，Ltd。

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