Interactions between trophoblast cells and the maternal and fetal circulation in the mouse placenta
Interactions between trophoblast cells and the maternal and fetal circulation in the mouse placenta
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DOI：
10.1006/dbio.2002.0773
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发表时间：
2002-10-15
影响因子：
2.7
通讯作者：
Cross, JC
中科院分区：
文献类型：
--
作者：
Adamson, SL;Lu, Y;Cross, JC
哺乳动物的胚胎与它们的母亲有着亲密的关系，尤其是与胎盘的脉管系统，胚胎从中获得生长所必需的营养。这是一个有趣的血管床，因为母体血管的数量和直径在妊娠期间发生了巨大的变化，在啮齿类动物和灵长类动物中，末端血液空间由胎盘滋养细胞而不是内皮细胞排列。由于缺乏对胎盘血管空间的解剖结构和母胎血管相互作用的一般性质的了解，旨在确定这些过程的潜在调节因子的小鼠分子遗传学研究受到了阻碍。为了解决这个问题，我们从胚胎日(E) 10.5到足月，通过制备塑料血管模型和植入部位的一系列组织学切片来检查小鼠胎盘的解剖结构。我们发现，携带母体血液进入子宫的每条桡动脉分支成5-10条扩张的螺旋动脉，位于子宫三角内，由子宫自然杀伤细胞（uNK）和基底蜕膜填充。由内皮层构成的螺旋状动脉在滋养层巨细胞层聚集在一起，流入几个由滋养层构成的直“管道”，将母体血液输送到胎盘底部。然后母体血液通过迷宫的绒毛间隙向胎盘的母体侧渗透，其方向与胎儿毛细血管血流的方向相反。滋养细胞以两种模式侵入子宫。表达滋养层巨细胞特异性基因Plf（编码增殖素）的大细胞在植入后早期以与螺旋动脉密切相关的模式侵入。这些血管周围/血管内滋养细胞仅在主巨细胞层上游150-300 μ m处被检测到。糖原滋养细胞侵袭基底蜕膜的第二种类型广泛存在于E12.5后。这些细胞不表达Plf，而是表达海绵滋养层细胞特异性基因Tpbp。在E10.5和E14.5之间，螺旋动脉明显扩张，并伴有弹性层和平滑肌细胞的缺乏。这些特征甚至在远离滋养层细胞入侵的子宫三角也很明显。相比之下，从内皮血管到滋养层血管的转变与滋养层巨细胞有关。此外，迷宫内母体血腔的形成依赖于绒毛膜尿囊形态发生，因此在Gcm1突变体中被破坏。这些研究提供了重要的见解如何胎胎盘单位相互作用与母体子宫内血管系统在怀孕期间的小鼠。(C) 2002 Elsevier Science （USA）。
Mammalian embryos have an intimate relationship with their mothers, particularly with the placental vasculature from which embryos obtain nutrients essential for growth. It is an interesting vascular bed because maternal vessel number and diameter change dramatically during gestation and, in rodents and primates, the terminal blood space becomes lined by placental trophoblast cells rather than endothelial cells. Molecular genetic studies in mice aimed at identifying potential regulators of these processes have been hampered by lack of understanding of the anatomy of the vascular spaces in the placenta and the general nature of maternal-fetal vascular interactions. To address this problem, we examined the anatomy of the mouse placenta by preparing plastic vascular casts and serial histological sections of implantation sites from embryonic day (E) 10.5 to term. We found that each radial artery carrying maternal blood into the uterus branched into 5-10 dilated spiral arteries located within the metrial triangle, populated by uterine natural killer (uNK) cells, and the decidua basalis. The endothelial-lined spiral arteries converged together at the trophoblast giant cell layer and emptied into a few straight, trophoblast-lined "canals" that carried maternal blood to the base of the placenta. Maternal blood then percolated back through the intervillous space of the labyrinth toward the maternal side of the placenta in a direction that is countercurrent to the direction of the fetal capillary blood flow. Trophoblast cells were found invading the uterus in two patterns. Large cells that expressed the trophoblast giant cell-specific gene Plf (encoding Proliferin) invaded during the early postimplantation period in a pattern tightly associated with spiral arteries. These peri/endovascular trophoblast were detected only similar to 150-300 mum upstream of the main giant cell layer. A second type of widespread interstitial invasion in the decidua basalis by glycogen trophoblast cells was detected after E12.5. These cells did not express Plf, but rather expressed the spongiotrophoblast-specific gene Tpbp. Dilation of the spiral arteries was obvious between E10.5 and E14.5 and was associated with a lack of elastic lamina and smooth muscle cells. These features were apparent even in the metrial triangle, a site far away from the invading trophoblast cells. By contrast, the transition from endothelium-lined artery to trophoblast-lined (hemochorial) blood space was associated with trophoblast giant cells. Moreover, the shaping of the maternal blood spaces within the labyrinth was dependent on chorioallantoic morphogenesis and therefore disrupted in Gcm1 mutants. These studies provide important insights into how the fetoplacental unit interacts with the maternal intrauterine vascular system during pregnancy in mice. (C) 2002 Elsevier Science (USA).