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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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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

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

Project description:Early-onset preeclampsia (EOPE) is a severe pregnancy complication associated with defective trophoblast differentiation and functions at implantation, but manifestation of its phenotypes is in late pregnancy. There is no reliable method for early prediction and treatment of EOPE. Adrenomedullin (ADM) is an abundant placental peptide in early pregnancy. Integrated single-cell sequencing and spatial transcriptomics confirm a high ADM expression in the human villous cytotrophoblast and syncytiotrophoblast. The levels of ADM in chorionic villi and serum were lower in first-trimester pregnant women who later developed EOPE 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 EOPE-like phenotypes. The EOPE-like phenotypes in a mouse PE model were reduced by a placenta-specific nanoparticle-based forced expression of ADM. Our study reveals the roles of trophoblastic ADM in placental development, EOPE pathogenesis, and its potential clinical uses.

| S-EPMC10624351 | biostudies-literature

BAP1 dysregulation impairs trophoblast differentiation and contributes to placental dysfunction in preeclampsia

Project description:This dataset profiles the proteomic effects of altering BAP1 expression in human trophoblast stem cells and trophoblast organoids. Samples from control, BAP1-overexpressing, and BAP1-knockdown conditions were analyzed by LC–MS/MS. DIA-NN–based quantification and differential analysis revealed BAP1-dependent changes affecting trophoblast differentiation, inflammatory signaling, and pathways linked to early-onset preeclampsia.

2026-03-24 | PXD071497 | Pride

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

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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

BAP1 dysregulation impairs trophoblast differentiation and contributes to placental dysfunction in preeclampsia

Project description:Preeclampsia, a life threatening hypertensive disorder of pregnancy, is a leading cause of maternal and perinatal morbidity and mortality. Its early onset form (EO PE), requiring delivery before 34 weeks of gestation, is particularly severe and closely linked to defective trophoblast differentiation. Here, we identify BRCA1-associated protein 1 (BAP1) and its cofactors ASXL2 and ASXL3 are upregulated in EO PE placentas. Enforced BAP1 expression in human trophoblast stem cells reinforced epithelial identity, enhanced adhesion, and impaired both extravillous trophoblast differentiation and syncytiotrophoblast formation. Integrated transcriptomic and proteomic analyses revealed suppression of lineage-specific pathways alongside maintenance of progenitor-like and pro-inflammatory signatures. In trophoblast organoids, excess of BAP1 disrupted syncytial maturation and induced interferon-driven pathways overlapping with EO PE transcriptomes. Together, these findings establish BAP1 as a key regulator of human trophoblast differentiation and implicate its dysregulation in the pathogenesis of EO PE, providing mechanistic insight into the cellular basis of placental dysfunction.

2026-03-27 | GSE311483 | GEO

FAK regulates trophoblast functions of invasion and proliferation through Rap1 pathway in preeclampsia

Project description:To explore the potential role of focal adhesion kinase (FAK) in trophoblast functions in early-onset preeclampsia (EOPE).We first examined expression and localization in placental tissue as well as in villus tissue during early pregnancy. Then, FAK activity was inhibited with Y15. The effects of FAK on the invasion and proliferation of trophoblast cells (HTR8/SVneo) were investigated. Transcriptomic and bioinformatics analyses were then used to predict the possible pathways by which FAK is involved in PE. Finally, we measured the expression of FAK in a PE mouse model. Transcriptomic and bioinformatics results suggest that Rap1 may be a downstream regulator of trophoblast FAK. In mouse models, we found reduced expression of FAK and Rap1 in the placenta of PE mice.

2025-07-10 | GSE271940 | GEO

TET1 modulates trophoblast function by regulation of ODC1 in preeclampsia

Project description:TET1 modulates trophoblast function by regulation of ODC1 in preeclampsia

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