Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Decidual stromal cell response to paracrine signals from the trophoblast

ABSTRACT: During the invasive phase of implantation, trophoblasts and maternal decidual stromal cells secrete products that regulate trophoblast differentiation and migration into the maternal endometrium. Paracrine interactions between the extravillous trophoblast and the maternal decidua are important for successful embryonic implantation, including establishing the placental vasculature, anchoring the placenta to the uterine wall, and promoting immuno-acceptance of the fetal allograph. Global cross-talk between the trophoblast and the decidua has not been elucidated to date, and the current study used a functional genomics approach to investigate these paracrine interactions. Our data demonstrate a significant induction of pro-inflammatory cytokines and chemokines, as well as angiogenic/static factors in decidualized endometrial stromal cells in response to trophoblast-secreted products. The data suggest that the trophoblast acts to alter the local immune environment of the decidua to facilitate the process of implantation and assure an enriched cytokine/chemokine environment, while limiting mitotic activity of the stromal cells during the invasive phase of implantation. Keywords: Gene expression arrays in human stromal cells

ORGANISM(S): Homo sapiens

PROVIDER: GSE5809 | GEO | 2006/09/18

SECONDARY ACCESSION(S): PRJNA97187

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Transcription profiling of human endometrial stromal cells treated with human trophoblasts vs. control, sampled at multiple time points to investigate stromal cell response to paracrine signals from the trophoblast

Project description:During the invasive phase of implantation, trophoblasts and maternal decidual stromal cells secrete products that regulate trophoblast differentiation and migration into the maternal endometrium. Paracrine interactions between the extravillous trophoblast and the maternal decidua are important for successful embryonic implantation, including establishing the placental vasculature, anchoring the placenta to the uterine wall, and promoting immuno-acceptance of the fetal allograph. Global cross-talk between the trophoblast and the decidua has not been elucidated to date, and the current study used a functional genomics approach to investigate these paracrine interactions. Human endometrial stromal cells were decidualized with progesterone and were further treated with conditioned media (CM) from human trophoblasts (TCM) or, as a control, with conditioned media (CCM) from non-decidualized stromal cells for 0, 3 and 12 hr. Total RNA was isolated and processed for analysis on whole genome, high density oligonucleotide arrays, containing 54,600 genes. Our data demonstrate a significant induction of pro-inflammatory cytokines and chemokines, as well as angiogenic/static factors in decidualized endometrial stromal cells in response to trophoblast-secreted products. The data suggest that the trophoblast acts to alter the local immune environment of the decidua to facilitate the process of implantation and assure an enriched cytokine/chemokine environment, while limiting mitotic activity of the stromal cells during the invasive phase of implantation.

2007-11-02 | E-GEOD-5809 | biostudies-arrayexpress

Transcriptomic of early embryonic invasion at implantation sites in a murine model.

Project description:Trophoblast Invasion is a complex mechanism that involves several genes and processes that are exquisitely regulated by the mother. Functional genomics has shown that immunomodulatory and proliferation are two essential key processes involved. Adult virgin B6CBA F1/J female mice were mated with CD1 fertile males to induce pregnancy (day 0=vaginal plug). Mice were sacrificed by cervical dislocation. Implantation and inter-implantation sites were divided by sharp dissection 6.5 days post-coitum (dpc) (n=3 mice). Uterine segments included uterine myometrium, stroma, and epithelium. Inter-implantation decidua (ID) were collected and Implantation sites also were divided by sharp dissection to separate extra-embryonic tissue (ET) from surrounding decidua (SD). From the embryo, only the invasive trophoblast formed by the ectoplacental cone was studied too.

2014-06-02 | E-GEOD-46732 | biostudies-arrayexpress

Preimplantation Factor Effect on Endometrial and Decidual Cells

2013-06-21 | GSE46326 | GEO

Proteomics of a microphysiological model of human trophoblast invasion during early embryo implantation

Project description:We have designed an implantation-on-a-chip device to model the invasion of specialized fetal extravillous trophoblasts (EVTs) from an implanting embryo into the maternal decidua. We profiled the proteome of the external factors secreted in the model, containing different cell population compositions: 1) Extravillous trophoblast monoculture - EVTs monoculture, 2) Endothelial cells monoculture - ECs monoculture, 3) EVTs + ECs coculture, and 4) EVTs, ECs, and decidualized stromal cells (DSCs) - triculture. The proteins were extracted using the MPLEx extraction method (Nakayasu et. al. PMCID: PMC5069757), digested with 1:50 (trypsin:protein, w:w) for 3 hr at 37 C. Solid Phase Extraction (SPE) was performed on the samples using 1 mL/50 mg columns from Phenomenex as previously described (PMCID: PMC7192326). Peptidic concentration was assayed using a BCA assay and 5 ul at 0.1 ug/ul were injected on the LC-MS/MS system. Data was searched with MaxQuant.

2021-02-16 | MSV000086888 | MassIVE

Preimplantation Factor Effect on Endometrial and Decidual Cells

Project description:Embryos secrete preimplantation factor (PIF), a peptide present in maternal circulation during viable pregnancy. We compared downstream synthetic PIF effect on gene expression in non-pregnant Human Endometrial Stromal Cell (HESC) and First Trimester Decidual cell (FTDC) culture to mimic the maternal intrauterine environment during embryo implantation and trophoblast invasion. Cells were cultured in triplicate with and without synthetic PIF for 24 hours. Cultured cells were then pooled for chip analysis. Altered gene expression relative to controls was assessed by Affymetrix microarray

2013-06-21 | E-GEOD-46326 | biostudies-arrayexpress

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

Project description:Placenta development involves complex molecular and cellular interactions between the maternal endometrium and the developing embryo, however, it is not clear what are the precise mechanisms regulating this maternal-fetal crosstalk. Using genetic and cell biological approaches, we have demonstrated that Ras-related C3 botulinum toxin substrate 1 (Rac1), a maternal factor expressed in decidual cells and is markedly elevated in mouse decidua on days 7 and 8 of gestation, regulates the secretory pathways that mediate stromal-endothelial and stromal-trophoblast crosstalk within a narrow temporal window during placenta development. Our study revealed that ablation of Rac1 did not affect the formation of the decidua but led to fetal loss in mid gestation accompanied by extensive hemorrhage. To gain insights into the molecular pathways affected by the loss of Rac1, we performed gene expression profiling which revealed that RAC1 signaling regulates the expression of genes involved in angiogenesis and vesicle trafficking. Consequently, the Rac1-null decidual cells exhibited impaired secretory functions that led to poor vascularization of the uterus and abnormal trophoblast expansion and placentation.

2017-02-09 | GSE70446 | GEO

Decidual NK cells Xiong et al 2013

Project description:Receptors of the KIR family on maternal Natural Killer cells in the decidua are believed to bind to Ligands such as HLA-C on trophoblast cells invading into the decidua from the placenta during early pregnancy. The resulting responses regulate the extent of trophoblast invasion. Genetic studies have implicated two members of the KIR family in particular as playing an important role: KIR2DL1 and KIR2DS1. The aim of this experiment was to determine what responses are generated when decidual NK cells bearing either KIR2DL1 or KIR2DS1 engage their HLA-C ligand.

2014-04-04 | E-MTAB-1784 | biostudies-arrayexpress

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

Project description: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.

2021-10-11 | GSE151329 | GEO

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

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data