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Direct analysis of the embryo-maternal interactions in a 3D biomimetic implantation niche

ABSTRACT: To decipher the crosstalk between the implanting mouse embryo and the maternal blood vessels we analysed the transcriptomes of the trophoblast and the endothelial cells using RNA-seq. Using laser-assisted microdissection, we isolated the mural trophectoderm of E4.5 (non-implanted embryo) and E4.75 blastocysts (attached to the uterine wall). As the invasive trophoblast giant cells (TGCs) at early egg cylinder stage (implanted embryo) are not accessible, we allowed the E4.5 mural TE to differentiate into TGCs in vitro for 3 days and then we proceeded with the transcriptional analysis. In addition, we analysed the transcriptome of the endothelial cells of the E5.5 decidua and the bEnd5 endothelial cell line. We found that the trophoblast activates the expression of a large repertoire of vascular receptors, ligands and cell adhesion molecules, compiling a network for communication with the maternal blood vessels.

ORGANISM(S): Mus musculus

PROVIDER: GSE151329 | GEO | 2021/10/11

REPOSITORIES: GEO

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Transcriptome analysis of bovine uninucleated trophoblast cells (UTC) and Trophoblast Giant Cells (TGC)

Project description:In the bovine placenta, intimate fetomaternal contacts are confined to multiple discrete structures termed placentomes. In the placentomes, widely ramified fetal chorionic villi interdigitate with corresponding maternal caruncular crypts. The trophoblast covering the chorionic villi is composed of uninucleate trophoblast cells (UTCs) and binucleate trophoblast giant cells (TGCs). TGCs are weakly invasive and capable of migrating toward the caruncular epithelium where they eventually fuse with single epithelial cells to form short-living trinucleate fetomaternal hybrid cells. Thereby, molecules of fetal origin are transported into the maternal compartment. The loss of TGCs due to fetomaternal hybrid cell formation is compensated by differentiation of UTCs into TGCs. We performed a genome-wide gene expression study of virtually pure UTCs and TGCs to to identify genes which are associated with trophoblast cell differentiation

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Trophoblast giant cell underrepresentation (CGH)

Project description:We characterized regions of underrepresentation that are specific to mouse polyploid trophoblast giant cells. We performed array Comparative Genomics Hybridization (aCGH) to examine copy number variation (CNV) in mouse polyploid trophoblast giant cells (TGCs). We performed the following experiments in duplicates to examine CNV during various stages of in vivo and in vitro TGC development: e9.5 TGCs vs. embryonic controls, e11.5 TGCs vs. embryonic controls, e13.5 TGCs vs. embryonic controls, e16.5 TGCs vs. embryonic controls, as well as TGCs cultured 3, 5 and 7 days vs. 2N trophoblast stem cells. We also performed the following controls to show that underrepresentation is only found in polypoid trophoblast giant cells and not in either 2N placental cell types nor in other types of polyploid cells: 2N placenta disk vs. embryonic controls, 2N trophoblast stem cells vs. embryonic stem cells, and polyploid Megakaryocytes vs. embryonic controls. When possible, we performed arrays with the test and control samples of opposite sex (F-female, M-male), as an internal control for the array.

2014-05-29 | E-GEOD-50543 | biostudies-arrayexpress

Adgrg1 is a New Transcriptional Target of Hand1 During Trophoblast Giant Cell Differentiation

Project description:The placenta, forming the maternal–fetal interface, is essential for the survival and development of the fetus. It has been shown that the basic helix-loop-helix (bHLH) transcription factor Hand1 plays an important role in trophoblast giant cells (TGCs) differentiation during placental development in mice. However, the underlying molecular mechanism remains elusive. We hereby report that Adgrg1 (GPR56), a G protein coupled receptor, was a new transcriptional target of Hand1. Hand1 activated the expression of Adgrg1 by binding to its promoter region during TGCs differentiation. Double in situ hybridization revealed co-expression of Hand1 and Adgrg1 in TGCs, and Adgrg1 was located to Prl2c2+ TGCs in the junctional zone of the placenta. Knockdown of Adgrg1 not only led to increased expression of Prl2c2, but also the improvement of cell migration during TGC differentiation. Moreover, the ligands of Adgrg1, Tgm2 and Col3a1, were expressed in Prl2c2+ TGCs located in the placental junctional zone and maternal spiral arteries, respectively, further providing preconditions for the function of Adgrg1 in TGCs. Collectively, these results demonstrate that Adgrg1 is a new transcriptional target of Hand1, affecting Prl2c2 expression and cell migration during TGCs differentiation. Tgm2 and Col3a1 may be involved in TGC differentiation regulated by Adgrg1 in the manners of autocrine or paracrine. As a transmembrane receptor, Adgrg1 perhaps could act as a potential therapeutic target for placental-associated diseases caused by abnormal trophoblast migration, providing new insights for the preventions and therapies of placenta-related diseases.

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Overexpression of trophoblast stem cell-enriched microRNAs promote trophoblast fate in embryonic stem cells.

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VE-cadherin is essential for trophoblast migration and endovascular invasion

Project description:Vascular endothelial (VE-)cadherin is a homotypic adhesion protein that is expressed selectively by ECs in which it enables formation of tight vessels and regulation of vascular permeability. Since VE-cadherin is also strongly expressed in placental trophoblasts, it is a prime candidate for a molecular mechanism of vascular mimicry by those cells. Here, we show that the VE-cadherin is required for trophoblast migration and endovascular invasion into the maternal decidua. VE-cadherin deficiency results in loss of spiral artery remodeling due to a lack of invasive trophoblasts, leading to decreased flow of maternal blood into the placenta, fetal growth retardation and death. Loss of trophoblast invasion prevents decidualization, extracellular matrix remodeling, and immune cell clearance. These studies identify VE-cadherin as essential for trophoblast migration and coordination of decidual changes during endovascular invasion. They further suggest endothelial proteins such as VE-cadherin that are expressed by trophoblasts may play functionally distinct roles that do not simply mimic those in ECs.

2021-11-30 | GSE189408 | GEO

SECRETORY PROTEOMIC RESPONSES OF ENDOMETRIAL EPITHELIAL CELLS TO TROPHOBLAST DERIVED EXTRACELLULAR VESICLES

Project description:Synchronized cross talk between embryo and endometrium during pre-implantation period is critical for establishment of pregnancy. Extracellular vesicels(EVs) of both embryo and endometrial origin are known to be integral in regulating embryo maternal communication during this time. However, exact molecular signalling pathways or factors that regulate the embryo endometrial communication during pre-conception period remains elusive. Here in this study extracellular vesicles from trophoblast cells were shown to modulate endometrial epithelial cell secretome in favour of embryo implantation and embryo development.

2023-10-24 | PXD040311 | Pride

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2012-08-02 | E-GEOD-31138 | biostudies-arrayexpress

The transcriptomic profile of human microvascular endothelial cells after exposure to preeclamptic or normotensive third trimester trophoblast debris

Project description:The human placenta is covered by a single multinucleated fetal cell, the syncytiotrophoblast, which is bathed in maternal blood. During all pregnancies, membrane enclosed extracellular vesicles derived from the syncytiotrophoblast are extruded into the maternal blood.The large size of these extracellular vesicles (diameter larger than 10 µm) is referred to as trophoblast debris in this study. We have shown in the past that trophoblast debris from first trimester can contribute to maternal cardiovascular physiological adaptations. This study aimed to characterise the transcriptional changes that occur in human vascular endothelial cells following exposure to preeclmaptic and normotensive trophoblast debris. Primeview human gene expression arrays were used to probe transcriptomic changes in human microvascular endothelial cells after exposure to preeclmaptic or normotensive trophoblast debris for 21 hours

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Validation of rapid embryo tracking using cell-free fetal DNA enriched from maternal circulation at 9 weeks gestation

Project description:Embryo DNA fingerprinting represents an important tool for tracking embryo-specific outcomes after multiple embryo transfer during IVF. The situation in which 2 embryos are transferred and only one implants represents a unique opportunity for the most well-controlled comparison of competent and incompetent embryos. Specifically, this design eliminates all patient-related variables from the comparison of embryos with or without reproductive potential. However, in order to determine which embryo implanted, the investigator must wait until newborn DNA is available upon delivery. This study validates a non-invasive fetal DNA fingerprinting method that reduces the time to identify which embryo implanted by approximately 31 weeks. Thirty-four patients were studied to determine if fingerprinting of fetal DNA extracted from maternal plasma at 9 gestational weeks concurred with the buccal DNA results obtained from the newborn after delivery. This validation required single nucleotide polymorphism (SNP) profiles on each couples’ preimplantation embryos, enriched fetal DNA from maternal plasma at 9 weeks gestation, and newborn DNA obtained from buccal swabs after delivery. The predictions from fetal DNA-based embryo tracking and gender assignments made at 9 weeks gestation were 100% consistent with standardized methods of assessment performed after term delivery. This study demonstrates the first validated fetal DNA fingerprinting method which predicts both gender and which embryo implanted at 9 weeks gestation following multiple embryo transfer.

2011-04-14 | GSE26404 | GEO

Gene expression profiling of mouse uterine decidua isolated on morning of day 8 of pregnancy

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2017-02-09 | GSE70446 | GEO

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