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Genome-wide analysis of gene expression in HTR8/SVneo cells treated with ZNF554 siRNA

ABSTRACT: Analysis of the effect of ZNF554 knock-down on genome-wide gene expression in trophoblastic cells. The hypothesis tested in the present study was that ZNF554 regulates the expression of genes involved in trophoblastic cell migration and invasion. The results provide important information on the functions of ZNF554 in trophoblastic cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE65940 | GEO | 2018/12/30

REPOSITORIES: GEO

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Genome-wide analysis of gene expression in BeWo cells treated with ZNF554 siRNA

Project description:Analysis of the effect of ZNF554 knock-down on genome-wide gene expression in BeWo trophoblast-like cells. The hypothesis tested in the present study was that ZNF554 regulates the expression of genes involved in key functions of trophoblastic cells. The results provide important information on the functions of ZNF554 in BeWo trophoblast-like cells.

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Comparative proteome of the BeWo and HTR8/SVneo trophoblastic cell lines

Project description:Here, we have undertaken comparative label-free quantitative (LFQ) proteomic profiling of the proteins expressed in BeWo and HTR8/SVneo cell lines using a mass spectrometry approach. We have identified 1557 proteins in total. 915 proteins were expressed in both cell lines including various transcription factors, chaperones and transport proteins. A further 338 and 304 proteins were uniquely expressed in BeWo and HTR8/SVneo cells respectively. Our bioinformatics analysis reflects the known epithelial and mesenchymal phenotypes of these cell models with principal differences in GO observed in ‘Cell junction’, ‘Catenin complex’ as well as ‘Cell adhesion’ and ‘Cell differentiation’. Our novel comparative proteomic analysis of these trophoblastic cell lines will set the stage for the use of trophoblastic cell lines for the study of pregnancy disorders and further research focusing on placental function.

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Transcriptomic analysis of human extravillous trophoblast cells (HTR8/Svneo) cultured as 3D spheroids and 2D monolayers

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5-Aza-dC treatment induces mesenchymal-to-epithelial transition in 1st trimester trophoblast cell line HTR8/SVneo.

Project description:Placental trophoblast invasion involves a cellular transition from epithelial to mesenchymal phenotype. Cytotrophoblasts undergo epithelial to mesenchymal transition (EMT) when differentiating into extravillous trophoblasts and gaining the capacity of invasion. In this research, we investigated the role of DNA methylation in trophoblasts during this EMT. First, using BeWo and HTR8/SVneo cell lines as models of cytotrophoblasts and extravillous trophoblasts, respectively, we analyzed the gene expression and DNA methylation status of the known epithelial marker genes, E-Cadherin and Cytokeratin7. We found that, in HTR8/SVneo cells, both genes were silenced and their promoters hypermethylated, as compared with the high-level gene expression and promoter hypomethylation observed in BeWo cells. This result suggests that dynamic DNA methylation of epithelial marker genes plays a critical role in the trophoblast EMT process. To verify these results, we treated HTR8/SVneo cells with 5-aza-dC, a known inhibitor of DNA methyltransferase, for three days. Five-Aza-dC treatment significantly increased the expression of epithelial marker genes and slightly decreased the expression of mesenchymal genes, as detected by qRT-PCR, immunocytochemistry and Western blot. Furthermore, 5-aza-dC treated HTR8/SVneo cells changed their morphology from mesenchymal into epithelial phenotype, indicating that 5-aza-dC induced mesenchymal to epithelial transition. Lastly, we examined the effect of 5-aza-dC on trophoblast migration and invasion capacity. We applied 5-aza-dC to HTR8/SVneo cells in trans-well cell migration and invasion assays and found that 5-aza-dC treatment decreased trophoblast migration and invasion capacity. In conclusion, DNA methylation of epithelial marker genes represents a molecular mechanism for the process of trophoblast EMT.

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Curcumin Protects Human Trophoblast HTR8/SVneo Cells from H2O2-Induced Oxidative Stress by Activating Nrf2 Signaling Pathway.

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Project description:Analysis of differentially expressed genes after siRNA mediated knock-down of the FET-family of proteins; the FUS, EWS, and TAF15 proteins. The FET-proteins are thought to function as transcription factors, and this hypothesis is tested in the present study. Results provide important information of the genes which expression are controlled by the FET-family of proteins.

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Transcriptional change of HTR8/Svneo cells over expressed with PLAC8-EGFP

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Adenosine A3 Receptor Mediates ERK1/2- and JNK-Dependent TNF-? Production in Toxoplasma gondii-Infected HTR8/SVneo Human Extravillous Trophoblast Cells.

Project description:Toxoplasma gondii is an intracellular parasite that causes severe disease when the infection occurs during pregnancy. Adenosine is a purine nucleoside involved in numerous physiological processes; however, the role of adenosine receptors in T. gondii-induced trophoblast cell function has not been investigated until now. The goal of the present study was to evaluate the intracellular signaling pathways regulated by adenosine receptors using a HTR-8/SVneo trophoblast cell model of T. gondii infection. HTR8/SVneo human extravillous trophoblast cells were infected with or without T. gondii and then evaluated for cell morphology, intracellular proliferation of the parasite, adenosine receptor expression, TNF-? production and mitogen-activated protein (MAP) kinase signaling pathways triggered by adenosine A3 receptor (A3AR). HTR8/SVneo cells infected with T. gondii exhibited an altered cytoskeletal changes, an increased infection rate and reduced viability in an infection time-dependent manner. T. gondii significantly promoted increased TNF-? production, A3AR protein levels and p38, ERK1/2 and JNK phosphorylation compared to those observed in uninfected control cells. Moreover, the inhibition of A3AR by A3AR siRNA transfection apparently suppressed the T. gondii infection-mediated upregulation of TNF-?, A3AR production and MAPK activation. In addition, T. gondii-promoted TNF-? secretion was dramatically attenuated by pretreatment with PD098059 or SP600125. These results indicate that A3AR-mediated activation of ERK1/2 and JNK positively regulates TNF-? secretion in T. gondii-infected HTR8/SVneo cells.

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