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Sexually dimorphic gene expression that overlaps maturation of type II pneumonocytes in fetal mouse lungs

机译:与胎儿小鼠肺中II型肺细胞成熟重叠的性二态基因表达

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摘要

BackgroundIn human, respiratory distress of the neonates, which occurs in prematurity, is prevalent in male. Late in gestation, maturation of type II pneumonocytes, and consequently the surge of surfactant synthesis are delayed in male fetuses compared with female fetuses. Although the presence of higher levels of androgens in male fetuses is thought to explain this sex difference, the identity of genes involved in lung maturation that are differentially modulated according to fetal sex is unknown. We have studied the sex difference in developing mouse lung by gene profiling during a three-day gestational window preceding and including the emergence of mature PTII cells (the surge of surfactant synthesis in the mouse occurs on GD 17.5).
机译:背景技术在人类中,早产中发生的新生儿呼吸窘迫在男性中很普遍。与女性胎儿相比,男性胎儿在妊娠后期,II型肺细胞的成熟以及因此表面活性剂合成的激增被延迟。尽管认为雄性胎儿中雄激素水平更高可以解释这种性别差异,但根据胎儿性别不同调节肺成熟的基因的身份尚不清楚。我们通过在三天的孕期窗之前和包括成熟的PTII细胞的出现(小鼠中表面活性剂合成的激增发生在GD 17.5上)的基因剖析研究了发育中的小鼠肺部的性别差异。

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