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

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

PROVIDER: PRJNA415391 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6202831_1.fastq.gz	Fastqsanger.gz
	SRR6202831_2.fastq.gz	Fastqsanger.gz
	SRR6202832_1.fastq.gz	Fastqsanger.gz
	SRR6202832_2.fastq.gz	Fastqsanger.gz
	SRR6202833_1.fastq.gz	Fastqsanger.gz

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

Project description:The goal of this this project was to study the transcriptional change when PLAC8-EGFP was over expressed in the trophoblast cell line, HTR8/Svneo.

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

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Effect of depletion of TET3 on gene expression of HTR8-SVneo trophoblast cells.

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Project description:In this study, we investigated the potential downstream target proteins in trophoblasts that were regulated by SIRT1 through modulation of acetylation. To this end, the IP products of SIRT1 in the lysate of human first-trimester villous tissue and HTR8/SVneo cells were subjected to proteomics analyses by LC-MS/MS.

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Project description:To investigate the role of METTL3-mediated m6A modification and mRNA translation, we performed m6A-sequencing and Ribosome-nascent chain (RNC)-RNA sequencing in high glucose treated control or METTL3 knockdown HTR8/SVneo cells.

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PM2.5 leads to adverse pregnancy outcomes by inducing trophoblast oxidative stress and mitochondrial apoptosis via KLF9/CYP1A1 transcriptional axis

Project description:Epidemiological studies have demonstrated that fine particulate matter (PM2.5) is associated with adverse obstetric and postnatal metabolic health outcomes, but the mechanism remains unclear. This study aimed to investigate the toxicological pathways by which PM2.5 damaged placental trophoblasts in vivo and in vitro. We confirmed that PM2.5 induced adverse gestational outcomes such as increased fetal mortality rates, decreased fetal number and weight, damaged placental structure, and increased apoptosis of trophoblasts. Additionally, PM2.5 induced dysfunction of the trophoblast cell line HTR8/SVneo, including in its proliferation, apoptosis, invasion, migration and angiogenesis. Moreover, we comprehensively analyzed the transcriptional landscape of HTR8/SVneo cells exposed to PM2.5 through RNA-Seq and observed that PM2.5 triggered overexpression of pathways involved in oxidative stress and mitochondrial apoptosis to damage HTR8/SVneo cell biological functions through CYP1A1. Mechanistically, PM2.5 stimulated KLF9, a transcription factor identified as binding to CYP1A1 promoter region, which further modulated the CYP1A1-driven downstream phenotypes. Together, this study demonstrated that the KLF9/CYP1A1 axis played a crucial role in the toxic progression of PM2.5 induced adverse pregnancy outcomes, suggesting adverse effects of environmental pollution on pregnant females and putative targeted therapeutic strategies.

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