Intrauterine Fate of Invasive Trophoblast Cells☆

Abstract

Invasion of trophoblast cells into the uterine spiral arteries and the uterine wall is characteristic of hemochorial placentation. In the rat, trophoblast cells penetrate through the uterine decidua and well into the metrial gland. In this report, we examined the fate of these invasive trophoblast cells following parturition. Invasive trophoblast endocrine cells were retained in the postpartum mesometrial uterus in the rat. The demise of invasive trophoblast cells was followed by the appearance of differentiated smooth muscle cells surrounding blood vessels previously lined by invasive trophoblast cells and an infiltration of macrophages. Regulation of intrauterine trophoblast cell fate was investigated following premature removal of the fetus or removal of the fetus and chorioallantoic placenta. The presence of the fetus affected the distribution of invasive trophoblast cells within the uterus but did not negatively impact their survival. Premature removal of all chorioallantoic placentas and associated fetuses from a uterus resulted in extensive removal of intrauterine trophoblast cells. In summary, the postpartum demise of intrauterine invasive trophoblast cells is a dynamic developmental event regulated in part by the removal of trophic signals emanating from the chorioallantoic placenta.

Maternal thyroid dysfunction affects placental profile of inflammatory mediators and the intrauterine trophoblast migration kinetics

“…This is important not only for the proper delivery of the fetus but also for the health of the mother and the success of subsequent pregnancies (Soares et al 2012). Increased intrauterine invasion of trophoblast cells during late gestation accompanied by a failure of their removal from the uterine decidua, in contrast to what was observed in T 4 -treated rats, is a pertinent cause of retained placenta, dystocia, and post partum hemorrhage in women and domestic animal species and can be fatal (Tantbirojn et al 2008, Rosario et al 2009). …”

Editor’s Highlight: Exposure to CrVI during Early Pregnancy Increases Oxidative Stress and Disrupts the Expression of Antioxidant Proteins in Placental Compartments

“…On the other hand, when TCs invade into uterine vasculature (trophoblastic vascular colonization), they are called endovascular TCs. These cells replace the endothelium of the uterine artery and are situated between the vasculature (Rosario et al, 2009). In the human, the invasive TC lineage is referred to as extravillous trophoblast (Velicky et al, 2016).…”

“…In the rat, as in human, specialized populations of TCs escape from the placenta and invade into the uterine stroma and establish relationships with uterine blood vessels (Rosario et al, 2009). Two populations of invading TCs, namely, interstitial and…”

“…endovascular TCs can be identified (Rosario et al, 2009). In order to identify the effects of CrVI on TC population, we performed immunofluorescence staining of TC marker cytokeratin in the placenta and metrial gland (MG).…”

Epigenetic control of cell invasion – the trophoblast model

“…It is believed that spongiotrophoblast cells are precursors of glycogen cells that are present in the second part of gestation in the rodent and are responsible for interstitional invasion (12) . These cells match interstitial trophoblast cells in humans, whereas giant trophoblast cells, analogous to the endovascular trophoblast, are responsible for the endovascular invasion of spiral arteries of the mother (13,14) .…”