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Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [RNA-Seq 2]

ABSTRACT: Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [RNA-Seq 2]

PROVIDER: PRJNA1157885 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30578200_1.fastq.gz	Fastqsanger.gz
	SRR30578200_2.fastq.gz	Fastqsanger.gz
	SRR30578201_1.fastq.gz	Fastqsanger.gz
	SRR30578201_2.fastq.gz	Fastqsanger.gz
	SRR30578202_1.fastq.gz	Fastqsanger.gz

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Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [ChIP-Seq]

Project description:The placenta develops alongside the embryo and nurtures fetal development to term. During the first stages of embryonic development, due to low blood circulation, the blood and ambient oxygen supply is normally very low (~1-2% O2) and gradually increases upon placental invasion. While a hypoxic environment is associated with stem cell self-renewal and proliferation, persistent hypoxia may have severe effects on differentiating cells and could be the underlying cause of placental disorders. We find that human trophoblast stem cells (TSC) thrive in low oxygen, whereas differentiation of syncytiotrophoblast (STB) and extravillous trophoblast (EVT) is negatively affected by hypoxic conditions. We find that the pro-differentiation factor GCM1 (human Glial Cell Missing-1) is downregulated in low oxygen, and there is substantial reduction of GCM1-regulated genes in hypoxic conditions. Knock-out of GCM1 in TSC caused impaired EVT and STB formation and function, reduced expression of genes that respond to differentiation, and resulted in maintenance of self-renewal genes. Treatment with a PI3K inhibitor reported to reduce GCM1 protein levels likewise counteracts spontaneous or directed differentiation. Chromatin immunoprecipitation of GCM1 showed enrichment of GCM1-specific binding near key transcription factors upregulated upon differentiation including the contact inhibition factor CDKN1C. Loss of GCM1 resulted in downregulation of CDKN1C and corresponding loss of contact inhibition, implicating GCM1 in regulation of this critical process.

2024-10-02 | GSE276590 | GEO

Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [ATAC-Seq]

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Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [RNA-Seq I]

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Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [RNA-Seq 2]

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Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [ChIP-Seq]

Project description:Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [ChIP-Seq]

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Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [ATAC-Seq]

Project description:Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [ATAC-Seq]

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Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [RNA-Seq I]

Project description:Hypoxia and loss of GCM1 expression prevents differentiation and contact inhibition in human trophoblast stem cells [RNA-Seq I]

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The multifaceted role of GCM1 during trophoblast differentiation in the human placenta

Project description:Human trophoblast stem cells were infected with lentivirus to knockdown the transcription factor GCM1. RNA-seq was then utilized to determine global transcriptomic changes between control and GCM1-deficient human trophoblasts either cultured as cytotrophoblasts or induced to form extravillous trophoblasts. This study provides insight into the molecular mechanisms regulating extavillous trophoblast development.

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To identify GCM1 novel target genes by chromatin immunoprecipitation-on-chip (ChIP-chip) analysis

Project description:In this study, we performed chromatin immunoprecipitation-on-chip (ChIP-chip) analysis and identified the gene for high-temperature requirement protein A4 (HtrA4) as a GCM1 target gene, which encodes a serine protease facilitating cleavage of fibronectin and invasion of placental cells. Importantly, HtrA4 is immunolocalized in EVTs at the maternal-fetal interface, and its expression is decreased by hypoxia and in preeclampsia, a pregnancy complication associated with placental hypoxia and shallow trophoblast invasion.

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Transcriptome analyses of trophoblast upon hypoxia or normoxia

Project description:The hypoxia inducible molecules are proposed to be one of many key regulators of first trimester trophoblast behavior, but the key mechanism mediating invasion of trophoblast cells is not very clear.

2024-03-01 | GSE128114 | GEO

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