Histology Atlas of the Developing Mouse Placenta

Abstract

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.

Kinetics of Placental Infection by Different Smooth Brucella Strains in Mice

“…It seems likely that an early inoculation during embryo implantation (4.5 DG) period [ 55 , 56 ] allows an effective colonisation of placental envelops, showing a progressive multiplication of 16M and Rev1, peaking at the end of gestation. It has been reported that Brucella localises preferentially in TGC [ 11 , 25 ], which are mainly placed at the junction and labyrinth layers [ 57 ].…”

“…The proliferation of TGC during these first stages of placental development seems to favour Brucella multiplication. Interestingly, 16M and B. suis bv2 counts decreased at 9.5 DG (5 days PI), the stage at which maternal blood enters the labyrinth [ 56 ]. This phenomenon could be explained by the increased irrigation of placental tissues facilitating cell-mediated immune response, which is followed by the marked cytokine release at 5 days PI.…”

Lipidomic Analysis of TRPC1 Ca2+-Permeable Channel-Knock Out Mouse Demonstrates a Vital Role in Placental Tissue Sphingolipid and Triacylglycerol Homeostasis Under Maternal High-Fat Diet

“…This is the first analysis of mouse placentae at two gestational time points that demonstrates the effect of HFD on lipidomic profiles. Our first measurement at E12.5 corresponds to the appearance of the first definitive placenta, while the second measurement point near E18.5 represents a fully functioning organ nearing the end of its lifespan, preparing for parturition ( 27 , 28 ). The visibly greater concentration of FC between the two diet arms at the early time point was not present by E18.5.…”

Ablation of SAMD1 in Mice Causes Failure of Embryonic Blood Vessel Maturation and Embryonic Lethality

“…This should not be surprising, since vessel development is similar in embryonic and extra-embryonic tissue [32][33][34] . Given that that by approximately E12.5 the de nitive placenta is mature 35 and the E12.5 embryos and extra-embryonic tissue appeared grossly normal, we conclude that embryonic lethality later than E12.5 is unlikely to have placental defects as a primary cause. We hypothesize therefore that lack of SAMD1 causes roughly simultaneous changes in the embryo, the yolk sac and the placental vasculature.…”