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Adrenomedullin has a pivotal role in trophoblast differentiation: A promising nanotechnology-based therapeutic target for preeclampsia.

ABSTRACT: Adrenomedullin has a pivotal role in trophoblast differentiation: A promising nanotechnology-based therapeutic target for preeclampsia.

PROVIDER: PRJNA991452 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25133300_1.fastq.gz	Fastqsanger.gz
	SRR25133300_2.fastq.gz	Fastqsanger.gz
	SRR25133301_1.fastq.gz	Fastqsanger.gz
	SRR25133301_2.fastq.gz	Fastqsanger.gz
	SRR25133302_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Adrenomedullin has a pivotal role in trophoblast differentiation: A promising nanotechnology-based therapeutic target for preeclampsia.

Project description:Preeclampsia (PE) is the leading cause of prenatal morbidity and mortality. It is associated with defective trophoblast functions at implantation, but manifestation of its phenotypes is in late pregnancy. There is no reliable method for early prediction and treatment of PE. Adrenomedullin (ADM) is an abundant placental peptide in early pregnancy. Here, integrated single-cell sequencing and spatial transcriptomics confirm a high ADM expression in the human villous cytotrophoblast. The levels of ADM in chorionic villi and serum were lower in first-trimester pregnant women who later developed PE than those with normotensive pregnancy. ADM stimulates differentiation of trophoblast stem cells and trophoblast organoids in vitro. In pregnant mice, placenta-specific ADM suppression led to PE-like phenotypes. The PE-like phenotypes in a mouse PE model were reduced by a novel placenta-specific nanoparticle-based forced expression of ADM. Our study reveals the roles of trophoblastic ADM in placental development, PE pathogenesis and its potential clinical uses.

2023-07-09 | GSE236475 | GEO

Diminished trophoblast differentiation in early onset preeclampsia

Project description:Comparison of genes associated with the EMT between undifferentiated cytotrophoblast cells (CTB) and differentiated extravillous trophoblast cells (EVT) from third trimester human placenta. Cells isolated from control (placenta previa) and cases (preeclampsia). Cells isolated by immunomagnetic separation using anti-integrin beta4 antibody to purify CTB and anti-HLA-G antibody to purify EVT.

2022-02-26 | GSE188313 | GEO

Diminished trophoblast differentiation in early onset preeclampsia

Project description:Diminished trophoblast differentiation in early onset preeclampsia

| PRJNA778240 | ENA

Hypoxia induces trophoblast migration and invasion gene pathways, a subset of which are reduced in preeclampsia

Project description:Placentation requires the proper regulation of extravillous trophoblast (EVT) migration and invasion into the decidua and maternal vasculature, processes which are initiated in physiologic hypoxic conditions. Abnormal EVT migration and/or invasion have been suggested to lead to pregnancy complications, such as preeclampsia. The objectives of this study are to determine how exposure to hypoxia impacts gene expression and cellular motility of first trimester trophoblasts, and to assess if expression of migration-associated genes is dysregulated in 2nd trimester chorionic villous samples (CVS) from preeclampsia pregnancies relative to CVS from healthy pregnancies. The 1st trimester trophoblast cell line, HTR8/SVneo, was used to investigate the relationship between hypoxia and Notch signaling in trophoblast migration and invasion. RNA sequencing and quantitative RT-PCR analyses show that exposure to hypoxia (2.5% O2) activates Notch signaling in HTR-8/SVneo. We demonstrate that exposure of HTR-8/SVneo to hypoxia induces expression of genes associated with cellular migration and invasion and increases HTR-8/SVneo cellular migration and invasion, whereas inhibition of gamma-secretase decreases Notch signaling and decreases HTR-8/SVneo migration and invasion. Analysis of RNA sequencing data from CVS of preeclampsia and uncomplicated pregnancies identified significant differentially expressed genes that are involved in cellular migration and invasion. Decreased expression of migration and invasion genes in CVS from preeclampsia pregnancies, may impair trophoblast migration and invasion in the 2nd trimester of pregnancy, resulting in the development of preeclampsia.

2021-08-05 | GSE155750 | GEO

Transcriptomic Profiling of Trophoblast Subpopulations in Severe Preeclampsia Reveals Novel Aspects of RNA Dysregulation

Project description:The maternal signs of preeclampsia, principally the new onset of high blood pressure, are thought to occur secondary to faulty placentation. Previous studies profiled the gene expression patterns of chorionic villi, the maternal-fetal interface or isolated cytotrophoblasts in this pregnancy complication. We theorized that transcriptomic analyses of trophoblast subpopulations in situ would give us new insights into the role of these cells in preeclampsia pathogenesis.

2017-01-24 | GSE93839 | GEO

iPSC-based modeling of preeclampsia identifies defects in extravillous trophoblast differentiation

Project description:Preeclampsia (PE) is a hypertensive pregnancy disorder with increased risk of maternal and fetal morbidity and mortality. Abnormal extravillous trophoblast (EVT) development and function is considered to be the underlying cause of PE, but has not previously been modeled in vitro. We previously derived induced pluripotent stem cells (iPSC) from placentas of PE patients and characterized abnormalities in formation of syncytiotrophoblast and responses to changes in oxygen tension. In this study, we converted these primed iPSC to naïve iPSC, then derived trophoblast stem cells (TSC) and EVT to evaluate molecular mechanisms underlying PE. We found that primed (but not naïve) iPSC-derived PE-EVT have reduced surface HLA-G, blunted invasive capacity, and altered EVT-specific gene expression. These abnormalities correlated with promotor hypermethylation of genes associated with the epithelial-mesenchymal transition pathway, specifically in primed-iPSC derived PE-EVT. Our findings indicate that abnormal epigenetic regulation might play a role in the PE pathogenesis.

2024-03-27 | GSE243579 | GEO

Early onset preeclampsia (EOPE) in a model for early stage human placental trophoblast

Project description:Early onset preeclampsia (EOPE) affects about 0.4% of pregnancies and is characterized by impaired trophoblast (TB) invasion, resulting in a poorly perfused placenta. Here we have used an in vitro model for mimicking early trophoblast development to determine how early placental development differs between normal pregnancies and those affected by EOPE. Induced pluripotent stem cells (iPSC) were generated from umbilical cords of infants born to mothers who had EOPE and from controls. These iPSC were converted to TB, by exposing them to BMP4 and inhibitors of ACTIVIN A and FGF2 signaling (BAP treatment), under 5 % and 20 % O2, hypothesizing that 20% O2 would act as a stressor. Two embryonic stem cell lines (ESC; H1 and H9), 8 control (CTL) iPSC and 14 EOPE iPSC were tested to assess how well the differentiated TB cells invaded through a Matrigel-coated membrane.

2018-12-31 | GSE119265 | GEO

iPSC-based modeling of preeclampsia identifies defects in extravillous trophoblast differentiation

Project description:iPSC-based modeling of preeclampsia identifies defects in extravillous trophoblast differentiation

| PRJNA1018965 | ENA

Preeclampsia is associated with reduced ISG15 levels impairing extravillous trophoblast invasion.

Project description:Preeclampsia is associated with reduced ISG15 levels impairing extravillous trophoblast invasion.

| PRJNA719566 | ENA

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

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