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Steroid Receptor Coactivator-2 Controls Human Extravillous Trophoblast Cell Proliferation, Migration, and Invasion

ABSTRACT: Steroid Receptor Coactivator-2 Controls Human Extravillous Trophoblast Cell Proliferation, Migration, and Invasion

PROVIDER: PRJNA1168193 | ENA |

REPOSITORIES: ENA

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Steroid Receptor Coactivator-2 Controls Human Extravillous Trophoblast Cell Proliferation, Migration, and Invasion

Project description:Abnormal placentation is a fundamental cause of pregnancy complications including preeclampsia, miscarriage, and intrauterine growth restriction. Proliferation, differentiation, migration, and invasion are key properties of trophoblast cells that regulate trophoblast functions. Imbalance of these cellular processes is linked to placental pathologies. Using HTR-8/SVneo immortalized human trophoblast cells, we demonstrate that steroid receptor coactivator-2 (SRC-2), a transcriptional regulator of nuclear receptors, is essential for extravillous trophoblast cell proliferation, migration, and invasion. Genome-wide transcriptomics identified an SRC-2–dependent transcriptome in HTR-8/SVneo cells that includes a diverse spectrum of proteins involved in placental tissue development and function. To emphasize the utility of this transcriptomics data set, we demonstrate that WNT family member 9A (WNT9A) is not only a molecular target of SRC-2 but also crucial for maintaining many of the cellular properties of human extravillous trophoblast cells.

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The pro-inflammatory cytokines IFN-α and TNF-α inhibit extravillous trophoblast invasion

Project description:Impaired trophoblast differentiation and invasion are a hallmark of severe pregnancy complications such as preeclampsia and fetal growth restriction. Women with immune-mediated inflammatory diseases, in particular systemic lupus erythematosus (SLE), have an increased risk for adverse pregnancy outcomes. These diseases are characterized by high activity of pro-inflammatory cytokines, such as interferon alpha (IFN-α) and tumor necrosis factor alpha (TNF-α). Here, we investigated the direct effects of these cytokines on extravillous trophoblast (EVT) differentiation and invasion, using trophoblast stem cells (TSCs), trophoblast organoids, and first-trimester placental and decidual tissue. While neither cytokine impaired EVT differentiation, both significantly reduced EVT invasion into extracellular matrix and/or maternal decidua. Transcriptomic analysis revealed cytokine-induced alterations in gene expression associated with epithelial-mesenchymal transition (EMT), a key process in EVT invasion. These findings suggest that elevated IFN-α and TNF-α levels may directly impair placental development by inhibiting EVT invasion, providing a mechanistic link between inflammatory conditions such SLE and adverse pregnancy outcomes.

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

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Steroid Receptor Coactivator-2 Regulated Transcriptome in Human Endometrial Stromal Cells

Project description:RNA-sequencing of mRNA isolated from in vitro decidualizaing human endometrial stromal cells with or without siRNA-mediated knockdown of steroid receptor coactivator-2/nuclear receptor coactivator 2 (SRC-2/NCOA2)

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GDF-11 stimulates human extravillous trophoblast cell invasion by upregulating ANGPTL4 expression

Project description:Proper regulation of extravillous trophoblast (EVT) cell invasion is critical for normal placental development and function. Growth differentiation factor 11 (GDF-11), a member of the transforming growth factor-β (TGF-β) superfamily, has been shown to promote EVT cell invasion, yet the underlying molecular mechanisms remain largely unclear. In this study, RNA sequencing identified angiopoietin-like 4 (ANGPTL4), a multifunctional secreted protein, as a novel downstream target of GDF-11. In vitro experiments demonstrated that GDF-11 significantly upregulated ANGPTL4 expression in both HTR-8/SVneo cells and primary human EVT cells. Mechanistically, we found that the type I TGF-β receptors ALK4 and ALK5 were essential for mediating the stimulatory effect of GDF-11 on ANGPTL4 expression. Further analysis revealed that SMAD3, but not SMAD2, was the key transcription factor involved in this process. Using both loss- and gain-of-function approaches, we demonstrated that ANGPTL4 was required for GDF-11-induced EVT cell invasion. Importantly, serum levels of GDF-11 were markedly reduced in patients with preeclampsia (PE), a pregnancy disorder associated with shallow trophoblast invasion and poor placentation. Together, our findings uncover a previously unrecognized GDF-11-ANGPTL4 signaling axis that regulates EVT cell invasion and provide new insight into the pathophysiology of PE.

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Role of YAP/TAZ-TEAD in human trophoblast

Project description:During placentation, placental cytotrophoblast cells differentiate into syncytiotrophoblast cells and extravillous trophoblast cells. In placenta, the expression of various genes is regulated by the Hippo pathway through the transcriptional coactivator YAP/TAZ-TEAD activity. To examine the effect of YAP/TAZ and/or TEAD on trophoblast differentiation, knockdown experiments were performed. Microarray analysis were performed to identify YAP/TAZ and/or TEAD target genes in human trophoblast.

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