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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:MicroRNAs (miRNAs) post-transcriptionally regulate a vast network of genes by inhibiting mRNA translation. Aberrant miRNA expression profiles have been implicated in pathologies and physiological processes including pregnancy and angiogenesis. Using our established model of implantation failure and spontaneous fetal loss in pigs (Sus scrofa), 236 miRNAs were profiled and compared between 1) non-pregnant and pregnant endometrium, 2) maternal and fetal tissues, and 3) viable and growth-arrested conceptus attachment sites by microarray and Real-Time PCR. Many significant differences in miRNA expression were observed between each of the aforementioned comparisons, and several were validated by PCR. Results indicated which miRNAs were important during pregnancy, which were elevated on the maternal or fetal side of the maternal-fetal interface, and they implicated the maternal expression of miR-10a, 27a, 29c, 323, 331-5p, 339-3p, 374b-5p, and 935 in the spontaneous loss observed in pigs. Several putative mRNA targets of the miRNAs (elevated in endometrium associated with arresting conceptuses) were assessed by quantitative Real-Time PCR and were depressed, supporting their regulation by miRNAs. Finally, targets were clustered by function to obtain ranked lists of gene networks that indicated which pathways/physiological processes might be important in non-pregnant (extracellular matrix factors) versus pregnant endometrium (nuclear transcription factor regulation), maternal (blood vessel development) versus fetal (neuronal differentiation) tissue, and healthy (extracellular matrix factors) versus arresting (GRAM domain) conceptus attachment sites. Overall, we demonstrate the presence of miRNAs on both sides of the maternal-fetal interface, implicate them in spontaneous fetal loss, and present a unique glimpse into the vast microRNAome of pregnancy.

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