The ability of the baby to receive nutrients and oxygen in utero depends on the healthy development of the placenta. For maternal blood to adequately perfuse the placenta, it dramatically alters the arteries in the uterus that supply it with nutrient-rich blood right from the start of pregnancy. Placental cells (trophoblasts) invade both into the tissue of the uterus and into the maternal blood vessels nearest to the site of implantation (the spiral arteries (SAs)) and transform these allowing a relatively high and steady flow of nutrient-rich blood to perfuse the placenta. Trophoblasts also form plugs that occlude SAs, preventing maternal blood flow to the placenta until the late first trimester, at which point these plugs dislodge or disintegrate. Here we present an agent-based model of trophoblast migration within plugged SAs to tease apart the impact of chemical signals and mechanical factors on trophoblast behaviour. The model supports our previous in vitro hypothesis that plugging of the maternal arteries in early pregnancy can act to promote trophoblast invasion by providing a 'low flow' environment and extends our understanding by suggesting 'weak spots' in plug structure can lead to plug degeneration, allowing increased blood flow through the materno-fetal circulation.

中文翻译：

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建立胎盘的孕妇血液供应：从基于代理的模型中了解堵塞，拔出和滋养层的行为。

婴儿在子宫内接受营养和氧气的能力取决于胎盘的健康发育。为了使孕妇的血液充分灌注胎盘，从怀孕开始，它就极大地改变了子宫动脉，为子宫提供了营养丰富的血液。胎盘细胞（滋养细胞）侵入子宫组织和最靠近植入部位的产妇血管（螺旋动脉（SAs）），并转化它们，从而允许相对较高和稳定的营养丰富血流灌注胎盘。滋养细胞还形成阻塞SA的栓塞，阻止孕妇血液流到胎盘直到妊娠晚期，这时这些栓塞会脱落或崩解。在这里，我们介绍了一种基于代理的滋养层在SA内迁移的模型，以梳理化学信号和机械因素对滋养层行为的影响。该模型支持我们先前的体外假说，即孕早期母体动脉的堵塞可通过提供“低流量”环境来促进滋养层的侵袭，并通过暗示堵塞结构中的“弱点”可导致堵塞退化来扩展我们的理解，允许血液流过胎儿的循环。