Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE70446 | GEO | 2017/02/09

SECONDARY ACCESSION(S): PRJNA288706

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

Decidual 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. 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

2006-09-18 | GSE5809 | 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

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

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. 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.

2016-03-14 | E-GEOD-74406 | biostudies-arrayexpress

Placental exosomes polarize human monocyte-derived macrophages to a decidual M2-like macrophage phenotype

Project description:Macrophages are abundant in uterine mucosa during the peri-implantation phase and early pregnancy. Decidual macrophages display dynamic changes alone with pregnancy progress: During the peri-implantation phase, macrophages displayed a pro-inflammatory phenotype which facilitates embryo implantation. While, In the late firster trimester and second trimester, decidual macrophages are anti-proinflammatory which are helpful to pregnancy maintenance. Alterations in the ratio of pro-inflammatory/anti-inflammatory decidual macrophages lead to abortion, preeclampsia, and preterm birth. Placenta-derived exosomes (pEXO) are critical in the immune cell modulation such as T cell apoptosis, NK activities, and T regulatory (Treg) differentiation. However, it is unknown whether placenta-derived exosomes contribute to decidual macrophage polarization during early pregnancy. Here we report that exosomes from the placenta explant stimulate M2 macrophage polarization via exosomal miRNA-30d-5p. Mechanistically, miRNA-30d-5p polarized macrophages to M2 phenotype by inhibiting HDAC9 expression. Furthermore, the conditioned medium of pEXO-treated macrophages promoted trophoblast migration and invasion. By contrast, conditioned medium impaired the ability of endothelial cell tube formation. However, pEXO-treated macrophages have no impact on T cell proliferation. Together, we demonstrated that pEXO promoted trophoblast migration and invasion, endothelial cell migration, and attenuation of endothelial cell tube formation by polarizing macrophage to decidua-like macrophage.

2021-09-16 | GSE184194 | GEO

Preimplantation Factor Effect on Endometrial and Decidual Cells

2013-06-21 | GSE46326 | GEO

Activation of the interferon pathway in trophoblast cells infected with SARS-CoV-2

Project description:Infection with SARS-CoV-2 in pregnancy has been associated with poor maternal and neonatal outcomes and placental defects. The placenta, which acts as a physical and immunological barrier at the maternal/fetal interface, is not established until the end of the first trimester. Therefore, localized viral infection of the trophoblast compartment early in gestation could trigger an inflammatory response resulting in altered placental function and consequent suboptimal conditions for fetal growth and development. In this study, we investigated the effect of SARS-CoV-2 infection in early gestation placentae using placenta-derived human trophoblast stem cells (TSC), a novel in vitro model, and their extra-villous trophoblast (EVT) and syncytiotrophoblast (STB) derivatives. Consistent with host viral entry protein expression, SARS-CoV-2 was able to productively replicate in TSC-derived STB and EVT but not undifferentiated TSC. Both early EVT and STB elicited an interferon-mediated innate immune response similar to other cells infected with this virus. Therefore, we have also shown that placenta derived TSCs are a robust in vitro model to investigate the effect of this viral infection in the trophoblast compartment of the early placenta. Overall, these results suggest that SARS-CoV-2 infection in early gestation can adversely affect placental development and that might occur via directly infecting the differentiated trophoblast compartment, thus posing a higher risk for poor pregnancy outcomes.

2023-10-14 | GSE216484 | GEO

Transcription profiling of human adipose tissue, decidua and placenta from patients with preeclampsia vs. unaffected indviduals reveals dysregulation of the circulating and tissue-based renin-angiotensin system in preeclampsia

Project description:Preeclampsia complicates more than 3% of all pregnancies in the United States and Europe. High-risk populations include women with diabetes, dyslipidemia, thrombotic disorders, hyperhomocysteinemia, hypertension, renal diseases, previous preeclampsia, twin pregnancies, and low socioeconomic status. In the latter case, the incidence may increase to 20% to 25%. Preeclampsia is a major cause of maternal and fetal morbidity and mortality. Preeclampsia is defined by systolic blood pressure of more than 140 mm Hg and diastolic blood pressure of more than 90 mm Hg after 20 weeks gestation in a previously normotensive patient, and new-onset proteinuria. Abnormal placentation associated with shallow trophoblast invasion (fetal cells from outer cell layer of the blastocyst) into endometrium (decidua) and improper spiral artery remodeling in the decidua are initial pathological steps. In this study we analyzed the renin-angiotensin system in adipose tissue, decidua and placenta from women with uneventful pregnancy and women with preeclampsia. We also analyzed the tissue by Affymetrix chips in a comparison study (control vs. preeclampsia) Experiment Overall Design: 6 affymetrix human expression chips (GPL570) were analyzed. Experiment Overall Design: They represent 3 tissues (pooled from 10 individuals each) from patients with preeclampsia and from patients with uneventful pregnancy (collected by cesaraen section). Tissues from patients with uneventful pregnancy are the controls in comparison to tissues of patients with preeclampsia.

2008-06-14 | E-GEOD-6573 | biostudies-arrayexpress

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

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