Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Single-cell RNA-seq transcriptome profiling of Prdm1+ lineages in E9.5 mouse placenta

ABSTRACT: Our goal was to transcriptionally profile Prdm1+ cell lineages of maternal and embryonic origin in mid-gestation mouse placenta in order to study vascular mimicry and additional processes in the placenta. Profiling of 61 single cells and 17 clusters of 2 or 3 cells chosen based on expression of Prdm1, a paternally inherited Prdm1-Venus fluorescent reporter, progenitor trophoblast marker Gjb3 and spiral artery trophoblast giant cell marker Prl7b1.

ORGANISM(S): Mus musculus

SUBMITTER: Andrew Nelson

PROVIDER: E-GEOD-74406 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Shared Molecules

Only show the datasets with similarity scores above: 0.5

Threshold

0.5

Similar Datasets

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

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

2016-03-14 | GSE74409 | GEO

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. 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.

2012-07-23 | E-GEOD-39584 | biostudies-arrayexpress

Single-cell RNA-seq transcriptome profiling of Prdm1+ lineages in E9.5 mouse placenta

Project description:Our goal was to transcriptionally profile Prdm1+ cell lineages of maternal and embryonic origin in mid-gestation mouse placenta in order to study vascular mimicry and additional processes in the placenta.

2016-03-14 | GSE74406 | GEO

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

2012-07-24 | GSE39584 | GEO

Prdm1

Project description:Prdm1

| PRJNA300302 | ENA

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

Gene expression profiles of trophoblast cell lines

Project description:Invasive extravillous trophoblasts (EVTs) of the human placenta are critically involved in successful pregnancy outcome since they remodel the uterine spiral arteries to increase blood flow and oxygen delivery to the placenta and the developing fetus. To gain more insights into their biological role different primary cell culture models are commonly utilised. However, access to early placental tissue may be limited and primary trophoblasts rapidly cease proliferation in vitro impairing genetic manipulation. Hence, trophoblastic cell lines have been widely used as surrogates to study EVT function. Although the cell lines share some molecular marker expression with their primary counterpart, it is unknown to what extent they recapture the invasive phenotype of EVT. Therefore, we here report the first thorough GeneChip analyses of SGHPL-5, HTR-8/SVneo, BeWo, JEG-3 and the novel ACH-3P trophoblast cells in comparison to previously analysed primary villous cytrophoblasts and extravillous trophoblasts. To identify EVT-specific gene expression signatures in trophoblast cell lines, we calcuted differentially expressed genes between pre-defined groups based on the distinct origins of the five trophoblast cell lines under investigation. Comparison 1 comprised EVT, HTR-8/Svneo and SGHPL-5 vs choriocarcinoma cells (ACH-3P, BeWo, JEG-3). Comparison 2 comprised EVT, ACH-3P, BeWo, JEG-3 vs extravillous trophoblast cell lines (HTR-8/SVneo, SGHPL-5).

2010-09-23 | E-GEOD-20510 | biostudies-arrayexpress

Intersection of Regulatory Pathways Controlling Hemostasis and Hemochorial Placentation [rat II]

Project description:Tissue factor pathway inhibitor (TFPI) is a prominent regulator of blood coagulation and an intriguing constituent of trophoblast cells situated at the maternal-fetal interface. The actions of TFPI extend beyond controlling hemostasis and directly affect trophoblast cell development. TFPI facilitates the differentiation of rat and human trophoblast stem cells into the invasive trophoblast/extravillous cell lineage and promotes intrauterine trophoblast invasion and trophoblast-guided uterine spiral artery remodeling at the maternal-fetal interface. Thus, TFPI is a conserved regulator of a fundamental event determining the efficacy of the hemochorial placenta.

2021-11-25 | GSE171754 | GEO

Intersection of Regulatory Pathways Controlling Hemostasis and Hemochorial Placentation [rat I]

2021-11-25 | GSE171753 | GEO