Isaac Sarah M, Qu Dawei, Adamson S Lee
Departments of Physiology, and Obstetrics and Gynaecology, University of Toronto, Toronto, ON, Canada; Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada.
Departments of Physiology, and Obstetrics and Gynaecology, University of Toronto, Toronto, ON, Canada; Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, ON, Canada.
Placenta. 2016 Oct;46:11-17. doi: 10.1016/j.placenta.2016.07.001. Epub 2016 Jul 7.
Placental examination is recommended when genetic mutations cause fetal lethality in mice. But how fetal death alters histomorphology of the surviving mouse placenta is not known.
Placentas were examined at E17.5 after fetectomy of 1-2 fetal mice per pregnancy at either embryonic day (E) 15.5 (N = 8; Fx-2 group) or E13.5 (N = 5; Fx-4 group), which left 12 ± 2 surviving fetuses per litter.
Fetectomy caused no changes in placental weights and no increases in placental hypoxia (pimonidazole staining). The size and cell morphology of the decidua and junctional zone regions were unchanged and, in the Fx-2 group, these regions became significantly less hypoxic. Significant changes in labyrinth volume included a 30% increase in the Fx-2 group and in both groups, a >50% decrease in % fetal blood space and >40% increase in % labyrinth tissue. Maternal blood sinusoid volume was unchanged. Cell death in the labyrinth was significantly increased (22-fold increase in TUNEL staining) whereas placental mRNA expression of the proliferation marker Mki67 was unchanged. mRNA expression of sFlt1 and Prl3b1 (mPL-II) was unchanged in the labyrinth and junctional zone tissues in the Fx-2 group and in whole placental tissue in the Fx-4 group.
Placental examination of the junctional zone and decidual regions after spontaneous fetal death in late gestation is likely to yield useful phenotypic information and abnormalities that may contribute to fetal death. In contrast, labyrinth abnormalities including increased tissue volume and reduced fetoplacental vascularity may not be due to genetic perturbation nor predate fetal death.
当基因突变导致小鼠胎儿死亡时，建议进行胎盘检查。但胎儿死亡如何改变存活小鼠胎盘的组织形态学尚不清楚。
在妊娠第15.5天（N = 8；Fx-2组）或第13.5天（N = 5；Fx-4组）对每窝1-2只胎儿进行胎仔切除术后，于胚胎第17.5天检查胎盘，每窝留下12±2只存活胎儿。
胎仔切除术未导致胎盘重量改变，也未增加胎盘缺氧（匹莫硝唑染色）。蜕膜和交界区区域的大小和细胞形态未改变，在Fx-2组中，这些区域的缺氧情况显著减轻。迷路体积有显著变化，Fx-2组增加了30%，两组中胎儿血腔百分比均减少>50%，迷路组织百分比增加>40%。母体血窦体积未改变。迷路中的细胞死亡显著增加（TUNEL染色增加22倍），而增殖标志物Mki67的胎盘mRNA表达未改变。Fx-2组迷路和交界区组织以及Fx-4组全胎盘组织中sFlt1和Prl3b1（mPL-II）的mRNA表达未改变。
妊娠晚期自然发生胎儿死亡后，对交界区和蜕膜区域进行胎盘检查可能会产生有用的表型信息和可能导致胎儿死亡的异常情况。相比之下，包括组织体积增加和胎盘血管减少在内的迷路异常可能不是由基因扰动引起的，也不是胎儿死亡之前就存在的。
