Ontology highlight
ABSTRACT:
PROVIDER: PRJNA649558 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Comprehensive quantitative proteomic study of human pre-implantation embryo stages reveal dynamic proteome landscape from M2, 8-cell and blastocyst stage, and during trophoblast stem cell (TS) differentiation. Identified key factors in early human embryos and lineage-specific trophoblast proteome profiles, correlated with transcriptomic analyses. This direct proteomic analysis provides a comprehensive analysis of the dynamic protein expression in human embryos during pre-implantation development and a powerful resource to enable further mechanistic studies on human trophoblast development and function.
2023-07-05 | MSV000092349 | MassIVE
Project description:This dataset is part of a study that aims to compare in vivo human trophoblast differentiation into EVTs to different in vitro trophoblast organoids using single-cell and single-nuclei RNA sequencing. This specific dataset includes scRNA-seq and snRNA-seq data from trophoblast stem cells (TSCs). Trophoblast stem cell (TSC) lines BTS5 and BTS11 derived by Okae and colleagues were grown as described previously (Okae et al. 2018) together with EVT differentiation media. This study shows that the main regulatory programs mediating EVT invasion in vivo are preserved in in vitro models of EVT differentiation from primary trophoblast organoids and trophoblast stem cells. Data for primary trophoblast organoids is available under E-MTAB-12650.
| EGAD00001010017 | EGA
Project description:Wnt signaling are essential for the maintenance and differentiation of stem/progenitor cells, including trophoblast stem cells during placental development. Hyper-activation of Wnt signaling has been shown to relate with human trophoblast diseases. However, litter is known about the impact and underlying mechanisms of excessive Wnt signaling during placental trophoblast development. In the present work, we found that Sfrp1,5 double mutant mouse exhibited disturbed trophoblast differentiation in the placental ectoplacental cone (EPC), where the precursors of secondary trophoblast giant cells (TGCs) and trophoblast cells in the spongiotrophoblast layer are located. Employing mouse models expressing a trunked β-catenin with exon 3 deletion globally and trophoblast-specifically, combining cultured trophoblast stem cells, we found that hyper-activation of canonical Wnt pathway exhausted the trophoblast precursor cells in the EPC, resulting in the overabundance of giant cells at the expense of spongiotrophoblast cells. Further examination uncovered that hyper-activation of canonical Wnt pathway disturbed trophoblast differentiation in the EPC via repressing Mash2 expression. Collectively, our findings demonstrate that appropriate canonical Wnt-β-catenin pathway is essential for EPC trophoblast differentiation during placental development. Our work also has high clinical relevance, since abnormal Wnt signaling are often associated with trophoblast-related diseases.
2020-03-06 | GSE146432 | GEO
Project description:Rcho-1 trophoblast stem cells can be maintained in a trophoblast stem cell state or induced to differentiate into trophoblast giant cells. During the differentiation process the PI3K pathway is constitutively activated. Microarray analysis of stem, differentiated and differentiated Rcho-1 trophoblast stem cells treated with the PI3K inhibitor LY294002.
2010-09-15 | GSE21938 | GEO
Project description:Trophectoderm-specific expression of Angiomotin (AMOT) in pre-implantation embryos followed by its unique expression in the post-implantation ectoplacental cone that harbors the trophoblast stem cell niche prompted our investigation on the function of AMOT in trophoblast cells. Using the in vitro trophoblast stem cell culture model, we established differentiation dependent up-regulation of AMOT expression in trophoblast cells. To understand the function of AMOT in trophoblast cells mass spectrometry-based proteomic analysis was employed to identify the AMOT interactome within the trophoblast proteome. This approach utilized immunoprecipitation of endogenous AMOT followed by fractionation on SDS-PAGE and subsequently subjecting the tryptic digested excised gel bands to mass spectrometry.
2021-11-03 | PXD019391 | Pride
Project description:Wnt signaling are essential for the maintenance and differentiation of stem/progenitor cells, including trophoblast stem cells during placental development. Hyper-activation of Wnt signaling has been shown to relate with human trophoblast diseases. However, litter is known about the impact and underlying mechanisms of excessive Wnt signaling during placental trophoblast development. In the present work, we found that Sfrp1,5 double mutant mouse exhibited disturbed trophoblast differentiation in the placental ectoplacental cone (EPC), where the precursors of secondary trophoblast giant cells (TGCs) and trophoblast cells in the spongiotrophoblast layer are located. Employing mouse models expressing a trunked β-catenin with exon 3 deletion globally and trophoblast-specifically, combining cultured trophoblast stem cells, we found that hyper-activation of canonical Wnt pathway exhausted the trophoblast precursor cells in the EPC, resulting in the overabundance of giant cells at the expense of spongiotrophoblast cells. Further examination uncovered that hyper-activation of canonical Wnt pathway disturbed trophoblast differentiation in the EPC via repressing Mash2 expression. Collectively, our findings demonstrate that appropriate canonical Wnt-β-catenin pathway is essential for EPC trophoblast differentiation during placental development. Our work also has high clinical relevance, since abnormal Wnt signaling are often associated with trophoblast-related diseases.
2020-03-06 | GSE146433 | GEO
Project description:Here, we demonstrate that upon inhibition of the Fgf/Erk pathway in mouse trophoblast stem cells (TSCs), the Ets2 repressor factor (Erf) interacts with components of the Nuclear Receptor Corepressor Complex 1 and 2 (NCoR1 and NCoR2). Upon attenuation of Fgf signalling, unphosphorylated, nuclear Erf recruits the NCoR1/2 complex to key trophoblast genes, brings about their transcriptional silencing and facilitates differentiation and placental development.
2023-04-26 | PXD037892 | Pride
Project description:The first lineage decisions during mouse development lead to establishment of embryonic and extraembryonic tissues. The transcription factor Cdx2 plays a central role by repressing pluripotency genes, such as Oct4 and promoting trophoblast fate at the blastocyst stage. Here we show that the transcription factor Gata3 is coexpressed with Cdx2 in the blastocyst and that overexpression of Gata3 in embryonic stem cells is sufficient to induce expression of trophoblast genes. Gata3 expression in the blastocyst does not depend on Cdx2, nor do Gata3 overexpressing cell lines require Cdx2 for expression of a subset of trophoblast genes. In the embryo, expression of Gata3, like Cdx2, depends on Tead4, and expression of both factors becomes restricted to nascent trophoblast by an Oct4-independent mechanism. These observations place Tead4 at the top of a trophoblast hierarchy, with Gata3 and Cdx2 acting downstream to induce expression of common and independent targets in this lineage. This SuperSeries is composed of the following subset Series: GSE12985: Differentiation time course of trophoblast stem cells GSE12986: Expression of Cdx2 or Gata3 in R1 mouse embryonic stem cells
2010-02-21 | E-GEOD-12999 | biostudies-arrayexpress
Project description:We characterized the trophoblast stem cell epigenome and gene expression profiles in rat and mouse. We profiled 5 histone modifications (+ chromatin input) using ChIP-Seq, and digital expression profiles (3' RNA-Seq) for trophoblast stem cells derived from rat and mouse. Furthermore, for mouse, we profiled key trophoblast stem cell factors Elf5, Cdx2, and Eomes. We found that enhancer regions (defined as distal regions of H3K27ac/H3K4me1 enrichment) were enriched for species-specific endogenous retroviral elements.
2012-12-04 | E-GEOD-42207 | biostudies-arrayexpress
Project description:Stem cells reside in specific niches providing stemness-maintaining environments. Thus, the regulated migration from these niches is associated with differentiation onset. However, mechanisms retaining stem cells in their niche remain poorly understood. Here, we show that the epigenetic regulator lysine-specific demethylase 1 (Lsd1) organises the trophoblast niche of the early mouse embryo by coordinating migration and invasion of trophoblast stem cells (TSCs). Lsd1 deficiency leads to the depletion of the stem cell pool resulting from precocious migration of TSCs. Migration is induced by premature expression of the transcription factor Ovol2 that is repressed by Lsd1 in undifferentiated wild-type TSCs. Increasing Ovol2 levels suffices to recapitulate the migration phenotype. Furthermore, Lsd1-deficient TSCs exhibit a developmental bias towards cells of the syncytiotrophoblast and impaired spongiotrophoblast and trophoblast giant cell differentiation. In summary, we describe that the epigenetic modifier Lsd1 coordinates placental development by retaining TSCs in their niche and directing trophoblast differentiation. Mouse trophoblast stem cells (TSCs) were isoloated from a single conditional Lsd1-deficient mouse (Lsd1tm1SchM-CM-<le). Deletion of Lsd1 was induced eight days before the collection of RNA by addition of 0.2 M-BM-5M 4OH-tamoxife. Cells were isolated at successive stages of differentiation for total RNA extraction and hybridization on Affymetrix microarrays. To that end, we harvested cells at three time-points: before induction of differentiation (d0), two days after induction of differentiation (d2), and four days after induction of differentiation (d4). Three replicates (1, 2, 3) for control (-) and Lsd1-deficeint (+) cells were included for each differentiation stage.
2014-01-17 | E-GEOD-38277 | biostudies-arrayexpress