Ontology highlight
ABSTRACT:
PROVIDER: PRJNA724881 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14319856_1.fastq.gz | Fastqsanger.gz | |||
| SRR14319856_2.fastq.gz | Fastqsanger.gz | |||
| SRR14319857_1.fastq.gz | Fastqsanger.gz | |||
| SRR14319857_2.fastq.gz | Fastqsanger.gz | |||
| SRR14319858_1.fastq.gz | Fastqsanger.gz |
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Project description:Transcriptomic Drivers of Differentiation, Maturation, and Polyploidy in Human Extravillous Trophoblast
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Project description:During pregnancy, normal extravillous trophoblast (EVT) invade the endomyometrium of the maternal uterus and remodel the spiral arteries to control blood supply and nutrient transfer. Recent reports have described first trimester EVT as polyploid and senescent. Here we extend these earlier reports by performing comprehensive profiling of the genomic organization and transcriptome of first trimester EVT and term EVT. We define pathways and gene regulatory networks involved in both initial differentiation and maturation of this important trophoblast lineage at the maternal-fetal interface. Our results suggest that like first trimester EVT, term EVT undergo senescence and endoreduplication, are primarily tetraploid, and lack high rates of copy number variations. Additionally, we have highlighted senescence and polyploidy-related genes, pathways, networks, and transcription factors that appeared to be important in normal EVT differentiation and maturation and have validated a critical role for the unfolded protein response in EVT differentiation.
2021-08-11 | GSE173369 | GEO
Project description:Placental development occurs in a low oxygen environment, yet how oxygen tension instructs differentiation of progenitor cytotrophoblasts (CTB) along the extravillous versus villous pathways remains incompletely understood. In particular, the role of low oxygen in early extravillous trophoblast (EVT) progenitor expansion and subsequent maturation has been difficult to assess due to the lack of models allowing sequential, high-resolution characterization. Using human trophoblast organoids and single-cell transcriptomics, we examined the effects of ambient (21%) and physiological (2–3%, 8%) oxygen on EVT and SCT differentiation. We show that low oxygen promotes the initial expansion of column CTB-like progenitors but restricts terminal EVT maturation. Conversely, we show that ambient oxygen drives the formation of EVT and syncytiotrophoblast. Stabilization of HIF-1 partially recapitulates the EVT maturation block but does not contribute to EVT progenitor expansion, indicating HIF-dependent and-independent contributions. These findings clarify how oxygen shapes EVT lineage progression and define HIF-1’s role in coordinating progenitor expansion versus maturation.
2026-09-01 | E-MTAB-16328 | biostudies-arrayexpress
Project description:During pregnancy, normal extravillous trophoblast (EVT) invade the endomyometrium of the maternal uterus and remodel the spiral arteries to control blood supply and nutrient transfer. Recent reports have described first trimester EVT as polyploid and senescent. Here we extend these earlier reports by performing comprehensive profiling of the genomic organization and transcriptome of first trimester EVT and term EVT. We define pathways and gene regulatory networks involved in both initial differentiation and maturation of this important trophoblast lineage at the maternal-fetal interface. Our results suggest that like first trimester EVT, term EVT undergo senescence and endoreduplication, are primarily tetraploid, and lack high rates of copy number variations. Additionally, we have highlighted senescence and polyploidy-related genes, pathways, networks, and transcription factors that appeared to be important in normal EVT differentiation and maturation and have validated a critical role for the unfolded protein response in EVT differentiation.
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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.
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Project description:The human placenta is built by trophoblast cells that fuse together, secrete hormones, and invade the uterus, and defects in these processes contribute to pregnancy disorders such as preeclampsia. Because cell-cell fusion and hormone secretion are inherently non-cell-autonomous processes, their regulators have remained inaccessible to conventional pooled CRISPR screens. Here, we developed an arrayed CRISPR screen in fusogenic BeWo trophoblasts that simultaneously quantifies fusion and hCG secretion across 412 gene perturbations. The screen revealed that these two hallmark functions of trophoblast differentiation are genetically separable. We characterized the strongest novel hit, ZBTB10, in trophoblast stem cells, organoids, and placental tissue and find that ZBTB10 is an essential regulator of human trophoblast differentiation. ZBTB10 is required for invasive extravillous trophoblast differentiation and supports syncytiotrophoblast maturation, establishing it as a cross-lineage regulator that both activates and represses distinct trophoblast fate programs. Together, these findings provide a genetic platform and phenotypic dissection of how regulatory networks control human placental development.
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