Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Pigment epithelium derived factor (PEDF): a novel trophoblast derived factor limiting feto-placental angiogenesis in late pregnancy

ABSTRACT: We hypothesized that the trophoblast secretes anti-angiogenic factors, which increase in late pregnancy to limit angiogenesis. Therefore, we determined the paracrine effect of primary human trophoblasts from early versus late pregnancy on the angiogenic potential of isolated feto-placental endothelial cells. We found that the expression and secretion of anti-angiogenic factors differs in early vs late pregnancy, and differentially affects feto-placental angiogenesis.

ORGANISM(S): Homo sapiens

PROVIDER: GSE69086 | GEO | 2017/01/01

SECONDARY ACCESSION(S): PRJNA284501

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

miRNA seq of feto-placental arterial endothelial cells (pfEC) after normal pregnancy vs pregnancy complicated by gestational diabetes (GDM)

Project description:We report that the effect of GDM on gene expression differs between feto-placental endothelial cells of male vs female progeny, i.e. after pregnancy with a male or female offspring.

2019-01-01 | GSE104297 | GEO

Methylome of Fetal and Maternal Monocytes and Macrophages at the Feto-Maternal Interface

Project description:Maternal and fetal monocytes and tissue macrophages (decidual macrophages, Hofbauer cells) at the feto-maternal interface have different methylome. Paired and balanced design. We compared maternal blood monocytes (MB) vs. cord blood monocytes (CB), maternal blood monocytes (MB) vs. decidual macrophages (Deci), cord blood monocytes (CB) vs placental macrophages (villi) and decidual macrophages (Deci) vs. placental macrophages (villi).

2011-11-15 | E-GEOD-31680 | biostudies-arrayexpress

Pigment epithelium-derived factor (PEDF): a novel trophoblast-derived factor limiting feto-placental angiogenesis in late pregnancy.

Project description:The rapidly expanding feto-placental vasculature needs tight control by paracrine and endocrine mechanisms. Here, we focused on paracrine influence by trophoblast, the placental epithelium. We aimed to identify differences in regulation of feto-placental angiogenesis in early versus late pregnancy. To this end, the effect of conditioned media (CM) from early and late pregnancy human trophoblast was tested on network formation, migration and proliferation of human feto-placental endothelial cells. Only CM of late pregnancy trophoblast reduced network formation and migration. Screening of trophoblast transcriptome for anti-angiogenic candidates identified pigment epithelium-derived factor (PEDF) with higher expression and protein secretion in late pregnancy trophoblast. Addition of a PEDF-neutralizing antibody restored the anti-angiogenic effect of CM from late pregnancy trophoblast. Notably, human recombinant PEDF reduced network formation only in combination with VEGF. Also in the CAM assay, the combination of PEDF with VEGF reduced branching of vessels below control levels. Analysis of phosphorylation of ERK1/2 and FAK, two key players in VEGF-induced proliferation and migration, revealed that PEDF altered VEGF signaling, while PEDF alone did not affect phosphorylation of ERK1/2 and FAK. These data suggest that the trophoblast-derived anti-angiogenic molecule PEDF is involved in restricting growth and expansion of the feto-placental endothelium predominantly in late pregnancy and targets to modulate the intracellular effect of VEGF.

| S-EPMC4930480 | biostudies-literature

Placental growth factor mediates pathological uterine vasculature by activating the NFAT5-SGK1 mechano-signaling axis in the endometrium: Implications for pre-eclampsia development.

Project description:After menstruation the uterine spiral arteries are repaired through angiogenesis. This process is tightly regulated by the paracrine communication between endometrial stromal cells (EnSCs) and endothelial cells. Any molecular aberration in these processes can lead to complications in pregnancy including miscarriage or pre-eclampsia (PE). Placental growth factor (PlGF) can increase cell stiffness contributing to pathological angiogenesis but the biomechanisms remain poorly understood. In this study, we investigated whether PlGF contributes to pathological uterine vasculature by disrupting EnSCs and endothelial paracrine communication. We observed that PlGF mediates a tonicity-independent activation of nuclear factor of activated T cells 5 (NFAT5) in EnSCs. NFAT5 activated downstream targets including SGK1, HIF-1α and VEGF-A. In depth characterization of PlGF - conditioned medium (CM) from EnSCs using mass spectrometry and ELISA methods revealed low VEGF-A and an abundance of extracellular matrix organization associated proteins. Secreted factors in PlGF-CM impeded normal angiogenic cues in endothelial cells (HUVECs) by downregulating Notch-VEGF signalling. Interestingly, PlGF-CM failed to support human placental (BeWo) cell invasion through HUVEC monolayer. Inhibition of SGK1 in EnSCs improved angiogenic effects in HUVECs and promoted BeWo invasion, revealing SGK1 as a key intermediate player modulating PlGF mediated anti-angiogenic signalling. Taken together, perturbed PlGF-NFAT5-SGK1 mechano-signaling in the endometrium can contribute to pathological uterine angiogenesis by negatively regulating EnSCs -endothelial crosstalk resulting in poor quality vessels in the uterine microenvironment. Taken together the signaling may impact on normal trophoblast invasion and thus placentation and, may be associated with an increased risk of complications such as PE.

2024-10-17 | PXD051697 | Pride

Human Feto-placental Arterial and Venous Endothelial Cells are Differentially Programmed by Gestational Diabetes Mellitus Resulting in Cell-specific Barrier Function

Project description:We performed genome-wide methylation analysis of primary feto-placental arterial and venous endothelial cells from healthy (AEC and VEC) and GDM complicated pregnancies (dAEC and dVEC). Parallel transcriptome analysis identified variation in gene expression linked to GDM-associated DNA methylation, implying a direct functional link. Pathway analysis found that genes altered by exposure to GDM clustered to functions associated with ’Cell Morphology’ and ’Cellular Movement’ in both AEC and VEC. Further functional analysis demonstrated that GDM exposed cells have altered actin organization and barrier function. Our data indicate that exposure to GDM programs atypical morphology and barrier function in feto-placental endothelial cells by DNA methylation and gene expression change. The effects differ between AEC and VEC, indicating a stringent cell-specific sensitivity to adverse exposures associated with developmental programming in utero.

2018-08-01 | GSE106099 | GEO

Human Feto-placental Arterial and Venous Endothelial Cells are Differentially Programmed by Gestational Diabetes Mellitus Resulting in Cell-specific Barrier Function Changes

2018-08-01 | GSE103552 | GEO

miRNA seq of feto-placental arterial endothelial cells (pfEC) after normal pregnancy vs pregnancy complicated by gestational diabetes (GDM)

Project description:miRNA seq of feto-placental arterial endothelial cells (pfEC) after normal pregnancy vs pregnancy complicated by gestational diabetes (GDM)

| PRJNA412262 | ENA

Human Cytomegalovirus modifies placental small extracellular vesicle secretion and composition to enhance infection of fetal recipient cells

Project description:Human cytomegalovirus (hCMV) primo-infection, reinfection and/or reactivation is a major issue during pregnancy and affects 1% of live births in western countries, making hCMV the most frequently transmitted virus in utero. Despite the extensive research conducted so far, the pathophysiology of this congenital infection remains unclear. Recently, increasing evidence point out the role of small extracellular vesicles (sEVs) in cell-cell communication underlying the feto-placenta-maternal dialogue during pregnancy. In this study, we examined the impact of hCMV infection on the protein composition and function of placental sEVs. We observed that infection of placental cells led to an alteration of protein composition of their secreted sEVs, suggesting that placental sEVs may acquire a proviral phenotype. Functional studies performed on fetal recipient cells, notably neural stem cells, confirmed the ability of sEVs produced by infected cells to facilitate further infection of naive recipient cells. Altogether, our study demonstrates that placental sEVs are key players of hCMV pathophysiology during congenital infection, and may favor the transmission of the virus towards the fetus.

2022-10-13 | PXD029146 | Pride

Fetus-derived IGF2 matches placental development to fetal demand [RNA-seq]

Project description:We used transcriptome analysis to identify genes transcriptionally disregulated in feto-placental endothelial cells from mutants with conditional deletion of Igf2 gene driven by the Meox2Cre.

2020-07-01 | GSE125351 | GEO

Fetus-derived IGF2 matches placental development to fetal demand II [RNA-seq]

2021-07-31 | GSE179549 | GEO