1285 PLACENTAL DEVELOPMENT IN THE TRISOMY 16 MOUSE
1285 PLACENTAL DEVELOPMENT IN THE TRISOMY 16 MOUSE
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第1285章 16三体小鼠的胎盘发育
DOI：
10.1203/00006450-198504000-01309
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发表时间：
1985
影响因子：
3.6
通讯作者：
J. Littlefield
中科院分区：
文献类型：
--
作者：
J. Gearhart;Mary Loster;G. Hatzidimitriou;J. Littlefield
Survival and development in utero involve the intimate interaction of mother, placenta, and embryo or fetus. However, when chromosomal aneuploidy occurs in the placenta and/or embryo or fetus, intrauterine growth retardation and fetal death are frequent outcomes of the pregnancy. Placental insufficiency may play a role in these events. Specifically, insufficiency of the fetal circulation in a hypoplastic placenta may result in underperfusion of the fetus. To examine this, we have studied the development of the placenta in trisomy 16 (Ts16) mice. Ts16 mice were selected because homology has been demonstrated between portions of mouse chromosome 16 and human chromosome 21, specifically that portion of HSA 21 implicated to cause Down Syndrome (DS) when present in triplicate.We examined 5 micron plastic section serial reconstructions of the placentas of Ts16 fetuses and their normal littermates from days 10 through 18 gestation. Morphometrically, the surface area ratio of fetal vasculature to that of the maternal sinuses was much less in the Ts16 fetus than its normal littermate but the ultrastructural characteristics of the placental barrier in the Ts16 fetus and its normal littermate were indistinguishable. The hypoplastic fetal vascular in the placenta could well lead to the underperfusion of the fetus, thus contributing to the aneuploid syndrome.
