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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Blimp1/Prdm1 governs terminal differentiation of endovascular trophoblast giant cells and defines multipotent progenitors in the developing placenta

ABSTRACT: Expression profiling of Prdm1 mutant E9.5 placenta was performed using Illumina whole genome V2 arrays. The hypothesis tested in the present study was that Blimp1 regulates the transcription of key genes involved in trophoblast differentiation. We demonstrate that the invading SpA-TGCs display robust Blimp1 expression and Blimp1 functional loss selectively disrupts specification of this discrete TGC sub-type. Transcriptional profiling experiments identified additional SpA-TGC lineage restricted marker genes that potentially regulate placental morphogenesis. Prdm1BEH/+ (Vincent et al., 2005) animals were intercrossed to generate null placental tissue. Total RNA obtained from 10 Prdm1+/+ and 11 Prdm1-/- E9.5 placenta samples was hybridized to Illumina WG6_V2 beadchips.

ORGANISM(S): Mus musculus

SUBMITTER: Arne Mould

PROVIDER: E-GEOD-39584 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Blimp1/Prdm1 governs terminal differentiation of endovascular trophoblast giant cells and defines multipotent progenitors in the developing placenta

Project description:Expression profiling of Prdm1 mutant E9.5 placenta was performed using Illumina whole genome V2 arrays. The hypothesis tested in the present study was that Blimp1 regulates the transcription of key genes involved in trophoblast differentiation. We demonstrate that the invading SpA-TGCs display robust Blimp1 expression and Blimp1 functional loss selectively disrupts specification of this discrete TGC sub-type. Transcriptional profiling experiments identified additional SpA-TGC lineage restricted marker genes that potentially regulate placental morphogenesis.

2012-07-24 | GSE39584 | GEO

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.

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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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Molecular function of Prdm1/Blimp1 in trophoblast giant cell differentiation.

Project description:Expression profiling of wild-type and Prdm1 null mouse trophoblast giant cell cultures using Illumina whole genome mouse V2 arrays. The hypothesis tested was that Prdm1/Blimp1 regulates expression of genes required for spiral artery trophoblast giant cell function. Prdm1 null and littermate control wild-type trophoblast stem cell clones were generated from blastocyst outgrowths. Total RNA was obtained from multiple replicates of four wild-type TS cell clones and four Prdm1 null TS cell clones differenitated for zero, two, four and six days by growth factor withdrawal and hybridized to Illumina WG6_V2 arrays

2016-03-14 | E-GEOD-74409 | biostudies-arrayexpress

The transcriptional repressor Blimp1/Prdm1 regulates post-natal reprogramming of intestinal enterocytes

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A Single Trophoblast Layer Acts as the Gatekeeper at the Endothelial-Hematopoietic Crossroad in the Placenta

Project description:During embryonic development the placental vasculature acts as a major hematopoietic niche, where endolthelial to hematopoietic transition ensures emergence of hematopoietic stem cells (HSCs). However, the molecular mechanisms that regulate the placental hematoendothelial niche are poorly understood. Using a parietal trophoblast giant cell (TGC)-specific knockout mouse model and single-cell RNA-sequencing, we show that the paracrine factors secreted by this single layer of TGCs are critical in the development of this niche. Disruptions in the TGC specific paracrine signaling leads to the loss of HSC population and the concomitant expansion of a KDR+/DLL4+/PROM1+ hematoendothelial cell-population in the placenta. Combining single-cell transcriptomics and receptor-ligand pair analyses, we also define the parietal TGC-dependent paracrine signaling network and identify Integrin signaling as a fundamental regulator of this process. Our study elucidates novel mechanisms by which non autonomous signaling from the primary parietal TGCs maintains the delicate placental hematopoietic-angiogenic balance and ensures embryonic and extraembryonic development.

2023-06-25 | GSE163286 | GEO

The development of mouse trophoblast cells at the single cell level

Project description:The placenta is a poorly understood yet vital support organ. Transcriptome analysis at single cell resolution can help us understand cell compositions, developmental processes, and physiological functions. Both mice and humans have the hemochorial placenta. Profiling the single cell transcriptome of the mouse placenta is necessary for deepening our knowledge of mammalian placentation.We systematically profiled single cell transcriptomes of mouse placentae every day from E7.5 to E14.5. After stringent filtering, 15682 mouse trophoblast cells were subjected to following transcriptome analysis. We noted that trophoblast cells underwent 3 main differentiation stages: E7.5-E8.5, E9.5-E10.5, and E11.5-E14.5. With the help of advanced computational technologies from Velocyto, PAGA, monocle, and SCENIC, we have updated the recognitions of several developmental events. Firstly, P-TGCs are suggested to only derive from EPC like cells. Secondary, sinusoid trophoblast and spongiotrophoblast all derived from EPC cells, and their cell fates have been determined before the chorioallantoic fusion. Sinusoid trophoblast cells were not derived from chorion. Thirdly, SpA-TGCs were suggested to be differentiated from spongiotrophoblast cells via Gly-T cells. Furthermore, new transcription factors have been found to play roles during the differentiation of trophoblast cells. Lastly, the expression of Ifnlr1 in chorion branch cells gradually increased during placentation, which reconfirmed that mature placenta can defend the Zika virus (ZIKV) through IFN signaling. We clarified the developmental histories of mouse trophoblast cells at the branch level, especially the differentiation of sinusoid branch trophoblast cells. Meanwhile, we offered a convincing data resource for the study of mammalian placentation and etiology analysis of pregnancy-associated diseases.

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microRNA (miRNA) expression profiles of murine polyploid trophoblast giant cells (TGCs) from day 9.5 implantation sites.

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2013-04-30 | E-GEOD-45784 | biostudies-arrayexpress

RNA expression profiles of murine polyploid trophoblast giant cells (TGCs) from day 9.5 implantation sites.

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