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Prenatally androgenized PCOS mice have ovary-independent uterine dysfunction and placental inflammation aggravated by high-fat diet

ABSTRACT: Prenatally androgenized PCOS mice have ovary-independent uterine dysfunction and placental inflammation aggravated by high-fat diet

PROVIDER: PRJNA1167202 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR30838200_1.fastq.gz	Fastqsanger.gz
	SRR30838200_2.fastq.gz	Fastqsanger.gz
	SRR30838201_1.fastq.gz	Fastqsanger.gz
	SRR30838201_2.fastq.gz	Fastqsanger.gz
	SRR30838202_1.fastq.gz	Fastqsanger.gz

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Prenatally androgenized PCOS mice have ovary-independent uterine dysfunction and placental inflammation aggravated by high-fat diet

Project description:Polycystic ovary syndrome (PCOS) is a common hyperandrogenic and metabolic condition in women. The syndrome is linked to subfertility and pregnancy complications, yet the independent effects of exposure to hyperandrogenism and obesity on endometrial function remain unclear. Here, PCOS-like mice were generated using prenatal androgenization (PNA) with dihydrotestosterone, followed by a prepubertal high-fat (HF) or standard diet. In ovariectomized mice, PNA impaired uterine closure during the implantation window, disrupted decidualization, and altered extracellular matrix- and inflammation-related gene expression. The effects were aggravated by HF diet. In naturally mated, ovary-intact mice, PNA and HF diet affected decidual and placental gene expression, suggestive of placental dysfunction and inflammation, and induced fetal growth restriction. This study underlines the role of the uterus in adverse pregnancy outcomes in PCOS and identifies possible underlying mechanisms for future studies. Pre-pregnancy interventions targeting metabolic health and hyperandrogenism should be the next steps to optimize PCOS pregnancy outcomes.

2025-04-10 | GSE278408 | GEO

MBD-seq in ovarian tissues of prenatally androgenized (PNA) mice

Project description:To investigate the molecular mechanism of PCOS underlying the hyperandrogenic phenotype, prenatally androgenized (PNA) mice were used to mimic this phenotype in women with PCOS. Methylated DNA binding domain sequencing (MBD-seq) and RNA-seq were performed on PNA mice (n=6) and control group (n=4) and validations were applied on ovarian samples from PNA mice (n=6) and control group (n=6) using MSP (methylation-specific PCR) and qPCR. The immunohistochemistry (IHC) and transmission electron microscope (TEM) profiling was separately conducted on tissue sections and granular cells of PNA mice (n=6) and control group (n=6). We identified 857 genes with differently methylated promoters and 3317 differently expressed genes in PNA mice and control group. We found that PCOS group had a down-regulation of Dnmt1 gene expression, accompanied by global hypomethylation compared with the control group. The promoter regions of Map3k1(mitogen-activated protein kinase kinase kinase 1) and Map1lc3ka (microtubule-associated protein1 light chain 3) were hypomethylated, accompanied by up-regulation of their mRNA expression, which may be involved in the regulation of PCOS through MAPK/p53 pathway activition and autophagy alteration.

2020-08-28 | GSE156960 | GEO

RNA-seq in ovarian tissues of prenatally androgenized (PNA) mice

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Ovarian tissues of prenatally androgenized (PNA) mice

Project description:Ovarian tissues of prenatally androgenized (PNA) mice

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Ovaries of PNA mice and controls

Project description:To investigate the etiology of the hyperandrogenic phenotype of polycystic ovary syndrome (PCOS), a prenatally androgenized (PNA) mouse model was validated and used for microarray analysis.

2017-11-01 | GSE103056 | GEO

MBD-seq in ovarian tissues of prenatally androgenized (PNA) mice

Project description:MBD-seq in ovarian tissues of prenatally androgenized (PNA) mice

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RNA-seq in ovarian tissues of prenatally androgenized (PNA) mice

Project description:RNA-seq in ovarian tissues of prenatally androgenized (PNA) mice

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miRNA-seq in ovarian tissues of prenatally androgenized (PNA) mice

Project description:miRNA-seq in ovarian tissues of prenatally androgenized (PNA) mice

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Epigenetic mechanism underlying the development of polycystic ovary syndrome (PCOS)-like phenotypes in prenatally androgenized rhesus monkeys.

Project description:The pathogenesis of polycystic ovary syndrome (PCOS) is poorly understood. PCOS-like phenotypes are produced by prenatal androgenization (PA) of female rhesus monkeys. We hypothesize that perturbation of the epigenome, through altered DNA methylation, is one of the mechanisms whereby PA reprograms monkeys to develop PCOS. Infant and adult visceral adipose tissues (VAT) harvested from 15 PA and 10 control monkeys were studied. Bisulfite treated samples were subjected to genome-wide CpG methylation analysis, designed to simultaneously measure methylation levels at 27,578 CpG sites. Analysis was carried out using Bayesian Classification with Singular Value Decomposition (BCSVD), testing all probes simultaneously in a single test. Stringent criteria were then applied to filter out invalid probes due to sequence dissimilarities between human probes and monkey DNA, and then mapped to the rhesus genome. This yielded differentially methylated loci between PA and control monkeys, 163 in infant VAT, and 325 in adult VAT (BCSVD P<0.05). Among these two sets of genes, we identified several significant pathways, including the antiproliferative role of TOB in T cell signaling and transforming growth factor-? (TGF-?) signaling. Our results suggest PA may modify DNA methylation patterns in both infant and adult VAT. This pilot study suggests that excess fetal androgen exposure in female nonhuman primates may predispose to PCOS via alteration of the epigenome, providing a novel avenue to understand PCOS in humans.

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Investigating the NPY/AgRP/GABA to GnRH Neuron Circuit in Prenatally Androgenized PCOS-Like Mice.

Project description:Polycystic ovary syndrome (PCOS), the most common form of anovulatory infertility, is associated with altered signaling within the hormone-sensitive neuronal network that regulates gonadotropin-releasing hormone (GnRH) neurons, leading to a pathological increase in GnRH secretion. Circuit remodeling is evident between GABAergic neurons in the arcuate nucleus (ARN) and GnRH neurons in a murine model of PCOS. One-third of ARN GABA neurons co-express neuropeptide Y (NPY), which has a known yet complex role in regulating GnRH neurons and reproductive function. Here, we investigated whether the NPY-expressing subpopulation (NPYARN) of ARN GABA neurons (GABAARN) is also affected in prenatally androgenized (PNA) PCOS-like NPYARN reporter mice [Agouti-related protein (AgRP)-Cre;τGFP]. PCOS-like mice and controls were generated by exposure to di-hydrotestosterone or vehicle (VEH) in late gestation. τGFP-expressing NPYARN neuron fiber appositions with GnRH neurons and gonadal steroid hormone receptor expression in τGFP-expressing NPYARN neurons were assessed using confocal microscopy. Although GnRH neurons received abundant close contacts from τGFP-expressing NPYARN neuron fibers, the number and density of putative inputs was not affected by prenatal androgen excess. NPYARN neurons did not co-express progesterone receptor or estrogen receptor α in either PNA or VEH mice. However, the proportion of NPYARN neurons co-expressing the androgen receptor was significantly elevated in PNA mice. Therefore, NPYARN neurons are not remodeled by prenatal androgen excess like the wider GABAARN population, indicating GABA-to-GnRH neuron circuit remodeling occurs in a presently unidentified non-NPY/AgRP population of GABAARN neurons. NPYARN neurons do, however, show independent changes in the form of elevated androgen sensitivity.

| S-EPMC7566551 | biostudies-literature

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