Similar Datasets
Project description:Our environment is replete with chemicals that can affect embryonic and extraembryonic development. Dioxins, such as 2,3,7,8-tetrachlorodibenzodioxin (TCDD), are compounds affecting development through the aryl hydrocarbon receptor (AHR). TCDD exposures can lead to placental adaptations and at higher doses pregnancy termination. Deep intrauterine endovascular trophoblast cell invasion was a prominent placentation site adaptation to TCDD. TCDD-mediated placental adaptations were dependent upon maternal AHR signaling but not placental or fetal AHR nor the presence of a prominent AHR target, cytochrome P450 1A1 (CYP1A1). At the placentation site, TCDD stimulated CYP1A1 transcription within endothelial cells but not trophoblast cells. Immune and trophoblast cell behaviors at the uterine-placental interface were guided by the actions of TCDD on endothelial cells. In summary, we have identified an AHR regulatory pathway activated by environmental stressors affecting uterine and trophoblast cell dynamics and the formation of the hemochorial placenta.
2021-06-18 | GSE178407 | GEO
Project description:Our environment is replete with chemicals that can affect embryonic and extraembryonic development. Dioxins, such as 2,3,7,8-tetrachlorodibenzodioxin (TCDD), are compounds affecting development through the aryl hydrocarbon receptor (AHR). TCDD exposures can lead to placental adaptations and at higher doses pregnancy termination. Deep intrauterine endovascular trophoblast cell invasion was a prominent placentation site adaptation to TCDD. TCDD-mediated placental adaptations were dependent upon maternal AHR signaling but not placental or fetal AHR nor the presence of a prominent AHR target, cytochrome P450 1A1 (CYP1A1). At the placentation site, TCDD stimulated CYP1A1 transcription within endothelial cells but not trophoblast cells. Immune and trophoblast cell behaviors at the uterine-placental interface were guided by the actions of TCDD on endothelial cells. In summary, we have identified an AHR regulatory pathway activated by environmental stressors affecting uterine and trophoblast cell dynamics and the formation of the hemochorial placenta.
2021-11-30 | GSE166659 | GEO
Project description:Our environment is replete with chemicals that can affect embryonic and extraembryonic development. Dioxins, such as 2,3,7,8-tetrachlorodibenzodioxin (TCDD), are compounds affecting development through the aryl hydrocarbon receptor (AHR). TCDD exposures can lead to placental adaptations and at higher doses pregnancy termination. Deep intrauterine endovascular trophoblast cell invasion was a prominent placentation site adaptation to TCDD. TCDD-mediated placental adaptations were dependent upon maternal AHR signaling but not placental or fetal AHR nor the presence of a prominent AHR target, cytochrome P450 1A1 (CYP1A1). At the placentation site, TCDD stimulated CYP1A1 transcription within endothelial cells but not trophoblast cells. Immune and trophoblast cell behaviors at the uterine-placental interface were guided by the actions of TCDD on endothelial cells. In summary, we have identified an AHR regulatory pathway activated by environmental stressors affecting uterine and trophoblast cell dynamics and the formation of the hemochorial placenta.
2021-11-30 | GSE166604 | GEO
Project description:Environmental Stressors Impact Placentation Through Actions On Trophoblast, Immune, and Endothelial Cell Dynamics
| PRJNA738892 | ENA
Project description:ENVIRONMENTAL STRESSORS IMPACT PLACENTATION THROUGH ACTIONS ON TROPHOBLAST, IMMUNE , AND ENDOTHELIAL CELL DYNAMICS
| PRJNA701551 | ENA
Project description:ENVIRONMENTAL STRESSORS IMPACT PLACENTATION THROUGH ACTIONS ON TROPHOBLAST, IMMUNE , AND ENDOTHELIAL CELL DYNAMICS [RNA-Seq]
| PRJNA701398 | ENA
Project description:ENVIRONMENTAL STRESSORS IMPACT PLACENTATION THROUGH ACTIONS ON TROPHOBLAST, IMMUNE , AND ENDOTHELIAL CELL DYNAMICS [scRNA-Seq]
| PRJNA701554 | ENA
Project description:In most mammals, placentation is critical for fetal development and pregnancy success. Exposure to marijuana during pregnancy has adverse effects, but whether the placenta is a target of cannabinoid/endocannabinoid signaling is not known. Using mice as a model system, we found that the endocannabinoid system is present in the ectoplacental cone and spongiotrophoblast cells. We also observed that aberrant endocannabinoid signaling confers premature trophoblast stem cell differentiation, and defective trophoblast development and invasion. These defects are reflected in retarded fetal development and compromised pregnancy outcome. Because the endocannabinoid system is conserved in mice and humans, our study suggests that endocannabinoid signaling is critical to placentation and pregnancy success in humans and implicates its potential significance in stem cell biology.
| S-EPMC2947871 | biostudies-other
Project description:During the peri-implantation period, multinucleated syncytia are formed in the sheep placenta. For over 20 years the scientific consensus has been that during trophoblast syncytialization in sheep, binucleate trophoblast giant cells (BNCs) differentiate from mononuclear trophoblast cells, and individual BNCs fuse with individual luminal epithelial (LE) cells to form trinucleate cells. These trophoblast-LE syncytial plaques then grow through continued BNC migration and fusion. Therefore, LE cells are thought to be incorporated into syncytial plaques. However, these ideas were based on electron microscopy studies, without benefit of molecular markers for BNC and LE cells to support conclusions. The aim of this study was to observe interactions between BNCs and uterine LE cells using immunohistochemical localization for molecular markers for BNCs and uterine LE cells. We performed immunofluorescence staining, laser capture microdissection, and TUNEL staining on the uterine-placental tissues of sheep during early placentation. We observed: (1) syncytial cells containing more than two nuclei within the trophoblast cell layer; (2) depolarized LE cells that express caspase 3 and stain positively for TUNEL; (3) engulfment of caspase 3-positive LE cells by trophoblast giant cells (TGCs) and empty spaces within the LE layer at sites of implantation; (4) rapid enlargement of syncytial plaques; and (5) E-cadherin and TUNEL-positive cells within the uterine stroma underlying degenerating LE was coincident with accumulation of CD45-positive cells at these sites. These data suggest that during early placentation: (1) fusion between trophoblasts is not limited to the formation of BNCs, and the term 'trophoblast giant cell (TGC)' may be appropriate; (2) LE cells undergo apoptosis; (3) apoptotic LE cells are eliminated by TGCs; (4) fusion is not limited to the incorporation of new BNCs but involves the lateral fusion between growing syncytial plaques; and (5) TGCs carry apoptotic LE cells away from the uterine-placental interface for elimination by immune cells within the stroma. These data indicate that uterine LE cells are not incorporated into syncytial plaques, but are engulfed and eliminated, and that early placentation in sheep is more similar to early placentation in humans than is currently understood in that both develop mononucleated cytotrophoblast and multinucleated syncytiotrophoblast layers of entirely placental origin. The elimination of LE cells by sheep TGCs might provide insights into elimination and penetration of LE cells during human embryo implantation.
| S-EPMC6769582 | biostudies-literature
Project description:We here review the evolution of invasive placentation in primates towards the deep penetration of the endometrium and its arteries in hominoids. The strepsirrhine primates (lemurs and lorises) have non-invasive, epitheliochorial placentation, although this is thought to be derived from a more invasive type. In haplorhine primates, there is differentiation of trophoblast at the blastocyst stage into syncytial and cellular trophoblast. Implantation involves syncytiotrophoblast that first removes the uterine epithelium then consolidates at the basal lamina before continuing into the stroma. In later stages of pregnancy, especially in Old World monkeys and apes, cytotrophoblast plays a greater role in the invasive process. Columns of trophoblast cells advance to the base of the implantation site where they spread out to form a cytotrophoblastic shell. In addition, cytotrophoblasts advance into the lumen of the spiral arteries. They are responsible for remodelling these vessels to form wide, low-resistance conduits. In human and great apes, there is additional invasion of the endometrium and its vessels by trophoblasts originating from the base of the anchoring villi. Deep trophoblast invasion that extends remodelling of the spiral arteries to segments in the inner myometrium evolved in the common ancestor of gorilla, chimp and human.
| S-EPMC4305171 | biostudies-literature