Histology Atlas of the Developing Mouse Placenta

The use of the mouse as a model organism is common in translational research. This mouse-human similarity holds true for placental development as well. Proper formation of the placenta is vital for development and survival of the maturing embryo. Placentation involves sequential steps with both embr...

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Bibliographic Details
Published inToxicologic pathology Vol. 50; no. 1; p. 60
Main Authors Elmore, Susan A, Cochran, Robert Z, Bolon, Brad, Lubeck, Beth, Mahler, Beth, Sabio, David, Ward, Jerrold M
Format Journal Article
LanguageEnglish
Published United States 01.01.2022
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Summary:The use of the mouse as a model organism is common in translational research. This mouse-human similarity holds true for placental development as well. Proper formation of the placenta is vital for development and survival of the maturing embryo. Placentation involves sequential steps with both embryonic and maternal cell lineages playing important roles. The first step in placental development is formation of the blastocyst wall (approximate embryonic days [E] 3.0-3.5). After implantation (∼E4.5), extraembryonic endoderm progressively lines the inner surface of the blastocyst wall (∼E4.5-5.0), forming the yolk sac that provides histiotrophic support to the embryo; subsequently, formation of the umbilical vessels (∼E8.5) supports transition to the chorioallantoic placenta and hemotrophic nutrition. The fully mature ("definitive") placenta is established by ∼E12.5. Abnormal placental development often leads to embryonic mortality, with the timing of death depending on when placental insufficiency takes place and which cells are involved. This comprehensive macroscopic and microscopic atlas highlights the key features of normal and abnormal mouse placental development from E4.5 to E18.5. This in-depth overview of a transient (and thus seldom-analyzed) developmental tissue should serve as a useful reference to aid researchers in identifying and describing mouse placental changes in engineered, induced, and spontaneous disease models.
ISSN:1533-1601
DOI:10.1177/01926233211042270