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Maternal microRNAs Linked To Birth Deficits Due To Prenatal Alcohol Exposure Are Dominant Modifiers of Gene Expression in Invasive Trophoblast Cells

ABSTRACT: Prenatal alcohol exposure (PAE) can impair placental development and result in fetal growth restriction. However, the underlying molecular mechanisms are unclear. We previously found that PAE in some, but not all pregnancies, resulted in significantly elevated circulating levels of 11 microRNAs (HEamiRNAs) in the 2nd trimester. This subgroup of PAE women experienced adverse infant birth outcomes due to PAE, Subsequently, these HEamiRNAs collectively but not individually, were found to inhibit a defined set of placental epithelial-mesenchymal transition (EMT) genes and, inhibited invasiveness of placental trophoblast cells. Here we extend these findings by performing whole-transcriptome analysis to dissect the contribution of ethanol compared to HEamiRNAs in HTR-8/SVneo cells, a model for invasive, human extravillous trophoblasts. We observed a large, distinct and statistically dominant effect of HEamiRNAs mimics on trophoblast transcript profiles irrespective of ethanol exposure, specifically on EMT, extracellular matrix, angiogenesis and immune signaling pathways among others. Weighted gene co-expression network analysis (WGCNA) identified additional placental growth networks related to epithelial cell proliferation and differentiation and MAPK/PI3K, Hippo and Rap1 signaling. This study provides a mechanistic framework to explain that the effects of PAE vary across pregnancies, because they are contingent in part, on the elevation key maternal circulating miRNAs.

ORGANISM(S): Homo sapiens

PROVIDER: GSE324021 | GEO | 2026/05/19

REPOSITORIES: GEO

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Differentially expressed genes in HTR-8/SVneo cell overexpressing miR-26a-5p modulate invasion and migration

Project description:Aberrant expression of microRNAs (miRNAs) is a critical factor in the pathogenesis of preeclampsia (PE). miR-26a-5p is a key regulatory miRNA that plays an important role in trophoblast cell function, which is essential during placental development. This study aims to investigate the impact of miR-26a-5p overexpression on the transcriptome of trophoblastic HTR-8/SVneo cells, a commonly used model for studying trophoblast functions in placentas collected from pregnancies complicated by PE. In this study, HTR-8/SVneo cells were transfected with 75 nM miR-26a-5p mimics, and RNA sequencing (RNA-seq) was employed to analyze alterations in gene expression.

2026-05-18 | GSE297810 | GEO

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

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.

2025-07-29 | GSE278677 | GEO

Gene expression profiles of trophoblast cell lines

Project description:Invasive extravillous trophoblasts (EVTs) of the human placenta are critically involved in successful pregnancy outcome since they remodel the uterine spiral arteries to increase blood flow and oxygen delivery to the placenta and the developing fetus. To gain more insights into their biological role different primary cell culture models are commonly utilised. However, access to early placental tissue may be limited and primary trophoblasts rapidly cease proliferation in vitro impairing genetic manipulation. Hence, trophoblastic cell lines have been widely used as surrogates to study EVT function. Although the cell lines share some molecular marker expression with their primary counterpart, it is unknown to what extent they recapture the invasive phenotype of EVT. Therefore, we here report the first thorough GeneChip analyses of SGHPL-5, HTR-8/SVneo, BeWo, JEG-3 and the novel ACH-3P trophoblast cells in comparison to previously analysed primary villous cytrophoblasts and extravillous trophoblasts. To identify EVT-specific gene expression signatures in trophoblast cell lines, we calcuted differentially expressed genes between pre-defined groups based on the distinct origins of the five trophoblast cell lines under investigation. Comparison 1 comprised EVT, HTR-8/Svneo and SGHPL-5 vs choriocarcinoma cells (ACH-3P, BeWo, JEG-3). Comparison 2 comprised EVT, ACH-3P, BeWo, JEG-3 vs extravillous trophoblast cell lines (HTR-8/SVneo, SGHPL-5).

2010-09-23 | E-GEOD-20510 | biostudies-arrayexpress

Illumina NovaSeq 6000 Mannose-B from Codonopsis Pilosula Modulates LAMB1 Expression to Enhance Trophoblast Function and Alleviate Subchorionic Hematoma

Project description:Introduction: This study investigates the active component Mannose-B from Codonopsis pilosula and its effect on human trophoblast cell function, particularly focusing on the regulation of Laminin Subunit Beta 1 (LAMB1) expression and its implications in subchorionic hematoma (SCH). Methods: Key genes involved in SCH pathology were identified through RNA sequencing and bioinformatics analysis. Network pharmacology was utilized to screen active components in Codonopsis pilosula and their critical targets. In vitro, HTR-8/Svneo cells were used to assess proliferation, migration, and invasion through CCK8, Transwell, and cell migration assays. A SCH rat model was established to evaluate changes in coagulation parameters, litter size, fetal viability, and fetal and placental weights. In vivo validation of Mannose-B's effects on LAMB1 expression and SCH pathology was performed using RT-qPCR and Western Blot. Results: Network pharmacology and molecular docking identified Mannose-B as an effective compound in Codonopsis pilosula, potentially beneficial for SCH treatment, with LAMB1 as a significant target. In vitro experiments showed that Mannose-B enhanced HTR-8/Svneo cell proliferation, migration, and invasion by reducing LAMB1 expression. In vivo experiments confirmed Mannose-B's inhibitory effect on placental LAMB1 expression and its potential in ameliorating SCH pathology. Conclusion: Mannose-B from Codonopsis pilosula inhibits LAMB1 expression, promoting human placental trophoblast cell proliferation, migration, and invasion, thereby mitigating the progression of SCH pathology.

2025-10-20 | PXD059213 | Pride

Using Genomic Signatures to Elucidate Individual and Mixture Effects of Inorganic Arsenic and Manganese in Placental Trophoblasts

Project description:HTR-8/SVneo human placental trophoblast cells were exposed to low-level environmentally relevant concentrations of iAs, Mn, and iAs-Mn mixtures. A microarray assay was performed to understand the changes and differences in gene expression in relation to single-metal and metal-mixtures

2023-08-14 | GSE240673 | GEO

Short communication: Upregulation of hypoxia/reoxygenation-induced Shc3 by downregulated miR-455-5p, suppresses trophoblasts implantation and is associated with placental inflammation and angiogenesis of preeclampsia

Project description:Preeclampsia is characterized by insufficient implantation of trophoblasts. It is relevant in the failure adaptation of trophoblasts to changes in the intrauterine embryo development environment. Fewer miRNAs have been reported on this. MiR-455-5p expressed lowly in preeclampsia but its role remains unknown. Combining cell and molecular biology methods, we suggested the function and relevant mechanisms of miR-455-5p and its potential target Shc3 in preeclampsia. In vitro, HTR-8/SVneo migrated and invaded more rapidly under H/R than in hypoxic or normoxic conditions when miR-455-5p was overexpressed. And the apoptosis of HTR-8/SVneo is in contrast to the migration and invasion in H/R. Shc3 was identified as a direct downstream target gene of miR-455-5p, where overexpression of this gene reversed the miR-455-5p impact, promoting apoptosis and suppressed invasion and migration of HTR-8/SVneo under H/R. Shc3 was highly expressed in H/R, but its level was low in isolated hypoxic or normoxic environments. Further, Shc3 overexpression is involved in placental inflammation and angiogenesis inhibition. Finally, we got the conclusion that the downregulation of miR-455-5p in preeclampsia contributes to the elevation of Shc3 in trophoblast, thereby deteriorating trophoblast cells implantation. The elevated Shc3 is associated with placental inflammation and angiogenesis inhibition. Shc3 serves as a potential biomarker for preeclampsia diagnosis and treatment.

2025-01-13 | GSE278196 | GEO

MIR193BHG inhibits the proliferation, migration and invasion of trophoblasts by upregulating p53

Project description:Aberrantexpression of long non-coding RNAs (lncRNAs) has been reported to play a crucial role in the biological function of trophoblasts and contribute to preeclampsia (PE). Our previous study demonstrated that MIR193BHG is increased in preeclamptic placental tissues. In this study, we further explored the effects of MIR193BHG on the function of trophoblast cells and attempted to elucidate its underlying molecular mechanisms. Results showed that MIR193BHG was predominantly localized in the nucleus of HTR-8/SVneo cells. Overexpression of MIR193BHG significantly inhibited proliferation, migration and invasion of HTR-8/SVneo cells, while increasing apoptosis. Knockdown of MIR193BHG produced opposite effects.Furthermore, overexpression of MIR193BHG led to significant increases in both mRNA and protein levels of p53 compared with the control group. More importantly, knockdown of p53 rescued the negative effects induced by overexpressed MIR193BHG on cell proliferation, migration, and invasion while partially counteracting its apoptotic effects on HTR-8/SVneo cells. In conclusion, our findings suggest that MIR193BHG played a critical role in the progression of PE by regulating the expression of p53 and may serve as a novel therapeutic target for PE.

2023-10-16 | GSE245279 | GEO

Gene expression in HTR-8/SVneo cells exposed to hypoxia or treated with sodium L-lactate

Project description:Chronical hypoxia is a common occurrence following reduced uteroplacental blood flow resulting from incomplete trophoblast invasion and abnormal vascular remodeling of the spiral arteries in PE. Hypoxia can lead to active glycolysis, which increases the production of lactate, a substrate for histone lactylation. To screen for genes that may be regulated by histone lactylation in PE placentas, we performed RNA-seq in HTR-8/SVneo cells under hypoxia or treated with sodium L-lactate. The results showed that 3578 genes were upregulated in the HTR-8/SVneo cells under hypoxia compared to those under normoxia, and 355 genes were upregulated in HTR-8/SVneo cells treated with sodium L-lactate compared to the control cells. 152 upregulated genes in the HTR-8/SVneo cells under hypoxia and those treated with sodium L-lactate overlapping.

2021-12-13 | GSE190694 | GEO

G protein-coupled estrogen receptor stimulates human trophoblast cell invasion via YAP-mediated ANGPTL4 expression

Project description:RNA sequencing was applied to HTR-8/SVneo human trophoblast cells in response to G1, an agonist of GPER, to identify the target genes of GPER.

2021-09-12 | GSE183879 | GEO

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