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Immune dysfunction mediated by the competitive endogenous RNA network in fetal side placental tissue of polycystic ovary syndrome

ABSTRACT: Immune dysfunction mediated by the competitive endogenous RNA network in fetal side placental tissue of polycystic ovary syndrome

PROVIDER: PRJNA1049348 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27109000.fastq.gz	Fastqsanger.gz
	SRR27109001.fastq.gz	Fastqsanger.gz
	SRR27108982_1.fastq.gz	Fastqsanger.gz
	SRR27108982_2.fastq.gz	Fastqsanger.gz
	SRR27108983_1.fastq.gz	Fastqsanger.gz

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Project description:Polycystic ovary syndrome (PCOS), a common endocrine and metabolic disorder affecting women in their reproductive years. Emerging evidence suggests that the maternal-fetal immune system is crucial for proper pregnancy. However, whether immune function is altered at the end of pregnancy in PCOS women and the underlying molecular mechanisms is currently unexplored. Herein, the basic maternal immune system was investigated (n = 136 in the control group; n = 103 in the PCOS group), and whole-transcriptome sequencing was carried out to quantify the mRNAs, miRNAs, and lncRNAs expression levels in fetal side placental tissue of women with PCOS. GO, KEGG, and GSEA analysis were employed for functional enrichment analysis. The process of identifying hub genes was conducted utilizing the protein-protein interaction network. CIBERSORT and Connectivity Map were deployed to determine immune cell infiltration and predict potential drugs, respectively. A network of mRNA-miRNA-lncRNA was constructed and then validated by qRT-PCR. First, red blood cell count, neutrophil count, lymphocyte count, hypersensitive C-reactive protein, and procalcitonin were significantly elevated, while placental growth factor was hindered in PCOS women. We identified 308 DEmRNAs, 77 DEmiRNAs, and 332 DElncRNAs in PCOS samples. Functional enrichment analysis revealed that there were significant changes observed in terms of the immune system, especially the chemokine pathway. Eight genes, including FOS, JUN, EGR1, CXCL10, CXCR1, CXCR2, CXCL11, and CXCL8, were considered as hub genes. Furthermore, the degree of infiltration of neutrophils was dramatically decreased in PCOS tissues. In total, 57 ceRNA events were finally obtained, and immune-related ceRNA networks were validated. Some potential drug candidates, such as enalapril and RS-100329, could have a function in PCOS therapy. This study represents the inaugural attempt to evaluate the immune system at the end of pregnancy and placental ceRNA networks in PCOS, indicating alterations in the chemokine pathway, which may impact fetal and placental growth, and provides new therapy targets.

Project description:Polycystic ovarian syndrome (PCOS) is the most common gynaecological endocrine disease in women of reproductive age, with a prevalence rate of more than 12%, and is characterised by sporadic ovulation or anovulation, hyperandrogenism and polycystic ovarian changes. Polycystic ovary syndrome has a complex clinical presentation and, in addition to affecting follicular development and reproductive endocrine levels in women of childbearing age, it also impairs early embryonic development, affecting pregnancy outcome and offspring health, but its pathogenesis is unclear. In this study, we constructed a mouse model of PCOS using late-gestational hyperandrogen exposure, and examined the reproductive endocrine phenotype and glycolipid metabolism phenotype in mice. We found that PCOS model mice exposed to dihydrotestosterone in late pregnancy could exhibit hyperandrogenic manifestations, presenting elevated vaginal-anal index and delayed puberty establishment, as well as disturbed estrous cycle in adulthood. Ovulation number, number of mature oocytes, fertilisation rate and number of blastocysts were significantly lower in PCOS model mice compared to control mice. Subsequently, we assessed the follicular development and embryonic development ability of the mice using superovulation and in vitro fertilisation experiments, and obtained preimplantation embryonic RNA expression profiles of PCOS mice by performing Smart-seqII RNA sequencing to explore the possible mechanisms by which PCOS affects preimplantation embryonic development and offspring health. Bioinformatics analyses showed that 160 differentially expressed genes were identified out of 12,165 genes in blastocyst samples from both groups of mice, of which calcium/calmodulin-dependent protein kinase II β (CAMK2B2), melanoma-associated antigen B2 (MAGEB2), and the ADAM metallopeptidase domain (Adam4) were significantly differentially between the polycystic ovary syndrome and control groups Expression. Functional enrichment analyses revealed that the differential genes were mainly associated with pathways such as glandular development, nephron development, organ development and receptor catabolism. Our current study highlights the deleterious effects of intrauterine exposure to hyperandrogenism on the expression of polycystic ovary syndrome in mice, as well as resulting in impaired development of their eggs and early embryos. These findings may provide valuable insights into the early prevention of polycystic ovary syndrome.

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Immune dysfunction mediated by the competitive endogenous RNA network in fetal side placental tissue of polycystic ovary syndrome

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