HAND1 knockdown disrupts trophoblast gene expression in vitro- human vascular endothelial cell
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA865264 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR20749676.fastq.gz | Fastqsanger.gz | |||
| SRR20749677.fastq.gz | Fastqsanger.gz | |||
| SRR20749678.fastq.gz | Fastqsanger.gz | |||
| SRR20749679.fastq.gz | Fastqsanger.gz | |||
| SRR20749680.fastq.gz | Fastqsanger.gz |
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Similar Datasets
Project description:HAND1 knockdown disrupts trophoblast global gene expression
| PRJNA865258 | ENA
Project description:Congenital heart disease (CHD) affects nearly 1% of births annually, and neonatal and perinatal outcomes in cases of CHD are strongly impacted by pregnancy outcomes. CHD pregnancies carry increased risk of developing pathologies of abnormal placentation including fetal growth restriction, preeclampsia, preterm birth, and stillbirth. HAND1 is a gene associated with CHD. In this study, we aimed characterize the mechanistic impacts of disrupting HAND1 on human vascular endothelial cell gene expression.
2022-08-03 | GSE210318 | GEO
Project description:Congenital heart disease (CHD) affects nearly 1% of births annually, and neonatal and perinatal outcomes in cases of CHD are strongly impacted by pregnancy outcomes. CHD pregnancies carry increased risk of developing pathologies of abnormal placentation including fetal growth restriction, preeclampsia, preterm birth, and stillbirth. HAND1 is a gene associated with CHD. In this study, we aimed characterize the mechanistic impacts of disrupting HAND1 on human placenta trophoblast cell lines.
2022-08-02 | GSE209620 | GEO
Project description:HAND1 knockdown disrupts trophoblast gene expression in vitro in Bewo cells
| PRJNA861834 | ENA
Project description:Congenital heart disease (CHD) affects nearly 1% of births annually, and CHD pregnancies carry increased risk of developing pathologies of abnormal placentation. We previously reported significant developmental impacts of disrupting Hand1, a gene associated with CHD, expression in placenta trophoblast and endothelial cells in multiple mouse models. In this study, we aimed to build upon this knowledge and characterize the mechanistic impacts of disrupting HAND1 on human placenta trophoblast and vascular endothelial cell gene expression. HAND1 gene expression was silenced in BeWo cells, a choriocarcinoma model of human cytotrophoblasts, (n = 3-9 passages) and isolated human placental microvascular endothelial cells (HPMVEC; n = 3 passages), with HAND1 siRNA for 96 h. Cells were harvested, mRNA isolated and RNA sequencing performed using the Illumina NextSeq 550 platform. Normalization and differential gene expression analyses were conducted using general linear modeling in edgeR packages. Statistical significance was determined using a log2 fold change of >1.0 or < -1.0 and unadjusted p-value ≤0.05. Panther DB was used for overrepresentation analysis, and String DB for protein association network analysis. There was downregulation of 664 genes, and upregulation of 59 genes in BeWo cells with direct HAND1 knockdown. Overrepresentation analysis identified disruption to pathways including cell differentiation, localization, and cell projection organization. In contrast, only seven genes were changed with direct HAND1 knockdown in HPMVECs. Disruption to HAND1 expression significantly alters gene expression profile in trophoblast but not endothelial cells. This data provides further evidence that future studies on genetic perturbations in CHDs should consider the extra-embryonic tissue in addition to the fetal heart.
| S-EPMC9875743 | biostudies-literature
Project description:Trophoblasts and amnion, as extra-embryonic lineages, can be differentiated from human pluripotent stem cells (PSCs) under defined culture conditions, but the regulatory mechanisms that coordinate the cell fate decisions between these lineages during PSC differentiation remain poorly defined. In this study, leveraging CRISPR/Cas9-mediated targeted screening and lineage reporter pluripotent stem cells (PSCs), we identified the transcription factor HAND1 as a critical determinant governing the divergence of trophoblast and amnion lineages in PSCs. Genetic ablation of HAND1 effectively suppressed the amnion differentiation capacity of EPSCs while enhancing their trophoblast differentiation potential. Conversely, ectopic overexpression of HAND1 have adverse effects. Notably, forced expression of HAND1 activated amnionic transcription program in human trophoblast stem cells (TSCs), demonstrating its lineage-reprogramming capability. Mechanistic analyses revealed that HAND1 cooperates with Wnt signaling pathway co-factors TCF/b-catenin to form a transcriptional complex that antagonistically regulates trophoblast- and amnion-associated gene networks. Collectively, our findings establish HAND1 as a pivotal regulator that orchestrates the fate choice between amnionic and trophoblast lineages during human PSC differentiation, providing insights into the molecular logic of extra-embryonic lineage specification.
2026-03-02 | GSE298710 | GEO
Project description:Trophoblasts and amnion, as extra-embryonic lineages, can be differentiated from human pluripotent stem cells (PSCs) under defined culture conditions, but the regulatory mechanisms that coordinate the cell fate decisions between these lineages during PSC differentiation remain poorly defined. In this study, leveraging CRISPR/Cas9-mediated targeted screening and lineage reporter pluripotent stem cells (PSCs), we identified the transcription factor HAND1 as a critical determinant governing the divergence of trophoblast and amnion lineages in PSCs. Genetic ablation of HAND1 effectively suppressed the amnion differentiation capacity of EPSCs while enhancing their trophoblast differentiation potential. Conversely, ectopic overexpression of HAND1 have adverse effects. Notably, forced expression of HAND1 activated amnionic transcription program in human trophoblast stem cells (TSCs), demonstrating its lineage-reprogramming capability. Mechanistic analyses revealed that HAND1 cooperates with Wnt signaling pathway co-factors TCF/b-catenin to form a transcriptional complex that antagonistically regulates trophoblast- and amnion-associated gene networks. Collectively, our findings establish HAND1 as a pivotal regulator that orchestrates the fate choice between amnionic and trophoblast lineages during human PSC differentiation, providing insights into the molecular logic of extra-embryonic lineage specification.
2026-03-02 | GSE299501 | GEO
Project description:The placenta, forming the maternal–fetal interface, is essential for the survival and development of the fetus. It has been shown that the basic helix-loop-helix (bHLH) transcription factor Hand1 plays an important role in trophoblast giant cells (TGCs) differentiation during placental development in mice. However, the underlying molecular mechanism remains elusive. We hereby report that Adgrg1 (GPR56), a G protein coupled receptor, was a new transcriptional target of Hand1. Hand1 activated the expression of Adgrg1 by binding to its promoter region during TGCs differentiation. Double in situ hybridization revealed co-expression of Hand1 and Adgrg1 in TGCs, and Adgrg1 was located to Prl2c2+ TGCs in the junctional zone of the placenta. Knockdown of Adgrg1 not only led to increased expression of Prl2c2, but also the improvement of cell migration during TGC differentiation. Moreover, the ligands of Adgrg1, Tgm2 and Col3a1, were expressed in Prl2c2+ TGCs located in the placental junctional zone and maternal spiral arteries, respectively, further providing preconditions for the function of Adgrg1 in TGCs. Collectively, these results demonstrate that Adgrg1 is a new transcriptional target of Hand1, affecting Prl2c2 expression and cell migration during TGCs differentiation. Tgm2 and Col3a1 may be involved in TGC differentiation regulated by Adgrg1 in the manners of autocrine or paracrine. As a transmembrane receptor, Adgrg1 perhaps could act as a potential therapeutic target for placental-associated diseases caused by abnormal trophoblast migration, providing new insights for the preventions and therapies of placenta-related diseases.
2022-01-12 | GSE193214 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-08-03 | GSE210319 | GEO
Project description:pcDNA3-HAND1-his was transfected into HEK293T cells and harvested after 48 hours. IMAC was carried out under denaturing conditions to enrich for HAND1,and samples were loaded onto SDS-PAGE gel with HAND1 gel band excised and submitted to LC-MS/MS.
2020-12-18 | PXD022407 | Pride