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EV-microRNA Signatures in Pregnant Women with Idiopathic Recurrent Pregnancy Loss: Deciphering MicroRNAome Pathway Networks at Feto-Maternal Interface

ABSTRACT: EV-microRNA Signatures in Pregnant Women with Idiopathic Recurrent Pregnancy Loss: Deciphering MicroRNAome Pathway Networks at Feto-Maternal Interface

PROVIDER: PRJNA1259415 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33446526.fastq.gz	Fastqsanger.gz
	SRR33446527.fastq.gz	Fastqsanger.gz
	SRR33446528.fastq.gz	Fastqsanger.gz
	SRR33446529.fastq.gz	Fastqsanger.gz
	SRR33446530.fastq.gz	Fastqsanger.gz

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EV-microRNA Signatures in Pregnant Women with Idiopathic Recurrent Pregnancy Loss: Deciphering MicroRNAome Pathway Networks at Feto-Maternal Interface

Project description:Despite extensive research in the past decade, the exact pathogenesis of recurrent pregnancy loss (RPL) remains unknown. At the time of pregnancy, human placenta releases microRNAs (miRNAs) enclosed in extracellular vesicles (EVs), which enter into maternal circulation and play an important role at feto-maternal interface to sustain a successful pregnancy. Aberrant expression of these miRNAs often results in adverse pregnancy complications. Therefore, studying the expression of these EV-miRNAs in maternal circulation could provide insights into the pathogenesis of RPL. miRNA sequencing revealed 66 (44 known and 22 novel) significantly DE miRNAs between RPL and healthy pregnant women.

2025-05-07 | GSE296460 | GEO

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Project description:Maternal and fetal monocytes and tissue macrophages (decidual macrophages, Hofbauer cells) at the feto-maternal interface have different methylome. Paired and balanced design. We compared maternal blood monocytes (MB) vs. cord blood monocytes (CB), maternal blood monocytes (MB) vs. decidual macrophages (Deci), cord blood monocytes (CB) vs placental macrophages (villi) and decidual macrophages (Deci) vs. placental macrophages (villi).

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Project description:Purpose: we tested the hypothesis that Hltf deletion in placenta either caused or exacerbated neonatal hypoglycemia via Hif-1α regulation of nutrient transporters. Methods: Individual samples [1 term placenta/sample x 5 biological replicates for test and control littermate female mice = 10 total samples] were flash frozen and sent to Otogenetics Corp. (Norcross, GA) for RNA-seq assays. Paired-end 100 nucleotide reads were aligned to genomic assembly mm10 and analyzed using the platform provided by DNAnexus, Inc. (Mountain View, CA). Results: There was no measureable evidence of uteroplacental dysfunction or fetal compromise. Conclusion: Our study is the first to show only the truncated Hltf isoform is expressed in E18.5 term placenta, and we identified a functional link between alternative splicing of Hltf and immunosuppression at the feto-maternal interface.

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