Kalisch-Smith J I, Simmons D G, Dickinson H, Moritz K M
School of Biomedical Sciences, The University of Queensland, St Lucia, QLD, 4072, Australia.
The Ritchie Centre, Hudson Institute of Medical Research and Department of Obstetrics and Gynaecology, Monash University, Australia.
Placenta. 2017 Jun;54:10-16. doi: 10.1016/j.placenta.2016.12.008. Epub 2016 Dec 8.
Exposure of the embryo or fetus to perturbations in utero can result in intrauterine growth restriction, a primary risk factor for the development of adult disease. However, despite similar exposures, males and females often have altered disease susceptibility or progression from different stages of life. Fetal growth is largely mediated by the placenta, which, like the fetus is genetically XX or XY. The placenta and its associated trophoblast lineages originate from the trophectoderm (TE) of the early embryo. Rodent models (rat, mouse, spiny mouse), have been used extensively to examine placenta development and these have demonstrated the growth trajectory of the placenta in females is generally slower compared to males, and also shows altered adaptive responses to stressful environments. These placental adaptations are likely to depend on the type of stressor, duration, severity and the window of exposure during development. Here we describe the divergent developmental pathways between the male and female placenta contributing to altered differentiation of the TE derived trophoblast subtypes, placental growth, and formation of the placental architecture. Our focus is primarily genetic or environmental perturbations in rodent models which show altered placental responsiveness between sexes. We suggest that perturbations during early placental development may have greater impact on viability and growth of the female fetus whilst those occurring later in gestation may preferentially affect the male fetus. This may be of great relevance to human pregnancies which result from assisted reproductive technologies or complications such as pre-eclampsia and diabetes.
胚胎或胎儿在子宫内受到干扰会导致子宫内生长受限，这是成年疾病发展的主要危险因素。然而，尽管暴露情况相似，但男性和女性在不同生命阶段的疾病易感性或病情进展往往有所不同。胎儿的生长很大程度上由胎盘介导，胎盘与胎儿一样，其基因组成是XX或XY。胎盘及其相关的滋养层谱系起源于早期胚胎的滋养外胚层（TE）。啮齿动物模型（大鼠、小鼠、刺毛鼠）已被广泛用于研究胎盘发育，这些研究表明，与雄性相比，雌性胎盘的生长轨迹通常较慢，并且对压力环境的适应性反应也有所改变。这些胎盘适应性变化可能取决于应激源的类型、持续时间、严重程度以及发育过程中的暴露窗口期。在这里，我们描述了雄性和雌性胎盘之间不同的发育途径，这些途径导致了TE衍生的滋养层亚型分化改变、胎盘生长以及胎盘结构的形成。我们主要关注啮齿动物模型中的遗传或环境干扰，这些干扰显示出两性之间胎盘反应性的改变。我们认为，胎盘早期发育过程中的干扰可能对雌性胎儿的生存能力和生长有更大影响，而妊娠后期发生的干扰可能优先影响雄性胎儿。这可能与辅助生殖技术导致的人类妊娠或子痫前期和糖尿病等并发症密切相关。
