The Role of Serum MicroRNA-6767-5p as a Biomarker for the Diagnosis of Polycystic Ovary Syndrome
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ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE86241 | GEO | 2016/08/31
SECONDARY ACCESSION(S): PRJNA341064
REPOSITORIES: GEO
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Project description:The effects of how obesity and elevated androgen levels in women with polycystic ovary syndrome (PCOS) affect their offspring are unclear. We found that daughters of PCOS mothers are more likely to be diagnosed with PCOS in a Swedish nationwide register-based cohort and a clinical case-control study from Chile. Further, female mice (F0) with PCOS-like traits induced by late gestation injection of dihydrotestosterone, with and without obesity, produced female F1–F3 offspring with a PCOS-like reproductive and metabolic phenotypes. Sequencing of single MII oocytes from F1–F3 offspring revealed common and unique altered gene expression across all generations. Notably, four genes were also differentially expressed in serum samples from daughters in the case-control study and unrelated women with PCOS. Our findings provide evidence of transgenerational effects in female offspring of PCOS mothers and identify possible candidate genes for the prediction of a PCOS phenotype in future generations.
2019-10-30 | GSE133100 | GEO
Project description:Polycystic ovary syndrome (PCOS) is a heterogeneous condition, of polyhedric pathogenesis and clinical presentation, defined by oligo-/anovulation, hyperandrogenism and/or polycystic ovaries. Metabolic complications are highly common also in patients suffering PCOS, including obesity, insulin resistance and type-2 diabetes, which severely compromise the clinical course of affected women. Yet, therapeutic options for PCOS remain mostly symptomatic and of limited efficacy for improving both metabolic and reproductive alterations. We report herein the hormonal, metabolic and gonadal responses to different GLP1-based multi-agonists, namely GLP1/Estrogen (GLP1/E), GLP1/GIP and GLP1/GIP/Glucagon, in two murine models of PCOS, with variable penetrance of metabolic and reproductive traits, and their comparison with metformin. Our data illustrate the superior efficacy of the di-agonist, GLP1/E, vs. other multi-agonists and metformin in the management of the metabolic complications of PCOS; GLP1/E was able to ameliorate also ovarian cyclicity in an ovulatory model of PCOS, without direct estrogenic uterotrophic effects. In keeping with GLP1-mediated brain targeting, label-free, quantitative proteomics revealed changes in common and distinct hypothalamic pathways in response to GLP1/E between the two PCOS models, as basis for differential efficiency. Altogether, our data set the basis for the use of GLP1-based multi-agonists, and particularly GLP1/E, in the personalized management of PCOS.
2024-10-02 | PXD044134 | Pride
Project description:Polycystic ovary syndrome (PCOS) is a common disorder encompassing reproductive, metabolic, and endocrine abnormalities, affecting 5 to 10% of women of reproductive age.To reveal the differences in proteomic profiles of follicular fluid between patients with and without PCOS and explore possible mechanisms underlying PCOS.Follicular fluid samples were collected from 9 infertile patients with PCOS and 9 infertile patients without PCOS. Quantitative proteomics analysis based on mass spectrometry was used to measure the protein levels and understand the protein networks. The tandem mass tag (TMT) based proteomics technology and bioinformatics analysis were used to determine the differentially expressed proteins(DEPs). : In this study, we have identified a total of 1216 proteins,these included 70 DEPs, in which 32 proteins were upregulated, and 38 proteins were downregulated. The bioinformatics analyses revealed multiple biological functions associated with these DEPs, some DEPs were enriched in the immune and metabolic-related biological processes in PCOS patients.
2022-10-14 | PXD031996 | Pride
Project description:Polycystic ovary syndrome (PCOS), the most common endocrine disease in reproductive-aged women, is associated with an increased prevalence and extent of coronary artery disease. However, the underlying mechanism remains unclear. Here, we observed that hearts from PCOS mice were characterized by increased total macrophage accumulation. Monocyte-derived macrophages were significantly increased in the hearts of PCOS mice owing to enhanced circulating monocyte supply. Compared with control mice, PCOS mice showed a significant increase in splenic monocyte output, associated with elevated hematopoietic progenitors in the spleen and sympathetic tone. Compared with non-PCOS animals, PCOS-induced mice showed significantly exacerbated atherosclerotic plaque development and post-MI cardiac remodeling. Conditional Vcam1 silencing in PCOS mice significantly suppressed cardiac inflammation and improved post-MI cardiac injury. Our data documented new mechanisms through which PCOS may affect cardiovascular health in women.
2024-01-02 | GSE238074 | GEO
Project description:Polycystic ovary syndrome (PCOS), the most common endocrine disease in reproductive-aged women, is associated with an increased prevalence and extent of coronary artery disease. However, the underlying mechanism remains unclear. Here, we observed that hearts from PCOS mice were characterized by increased total macrophage accumulation. Monocyte-derived macrophages were significantly increased in the hearts of PCOS mice owing to enhanced circulating monocyte supply. Compared with control mice, PCOS mice showed a significant increase in splenic monocyte output, associated with elevated hematopoietic progenitors in the spleen and sympathetic tone. Compared with non-PCOS animals, PCOS-induced mice showed significantly exacerbated atherosclerotic plaque development and post-MI cardiac remodeling. Conditional Vcam1 silencing in PCOS mice significantly suppressed cardiac inflammation and improved post-MI cardiac injury. Our data documented new mechanisms through which PCOS may affect cardiovascular health in women.
2024-01-02 | GSE238073 | GEO
Project description:Polycystic ovary syndrome (PCOS), the most common endocrine disease in reproductive-aged women, is associated with an increased prevalence and extent of coronary artery disease. However, the underlying mechanism remains unclear. Here, we observed that hearts from PCOS mice were characterized by increased total macrophage accumulation. Monocyte-derived macrophages were significantly increased in the hearts of PCOS mice owing to enhanced circulating monocyte supply. Compared with control mice, PCOS mice showed a significant increase in splenic monocyte output, associated with elevated hematopoietic progenitors in the spleen and sympathetic tone. Compared with non-PCOS animals, PCOS-induced mice showed significantly exacerbated atherosclerotic plaque development and post-MI cardiac remodeling. Conditional Vcam1 silencing in PCOS mice significantly suppressed cardiac inflammation and improved post-MI cardiac injury. Our data documented new mechanisms through which PCOS may affect cardiovascular health in women.
2024-01-02 | GSE238072 | GEO
Project description:Polycystic ovary syndrome (PCOS) is a heterogeneous disorder, and the underlying molecular mechanisms are not clear. To date, few studies have been conducted on the altered expression of serum microRNAs (miRNAs) in women with PCOS. The present study was performed to examine the role of the serum miRNA as a biomarker for the diagnosis of PCOS and its relationship with metabolic and reproductive traits.A cross-sectional comparison was made in 21 women with PCOS and age- and body mass index (BMI)- matched 21 healthy women in an academic center laboratory between December 2008 and October 2010. We selected miRNAs that were more than 1.5-fold up-regulated or less than 0.67-fold down-regulated in women with PCOS compared with controls using the SurePrint G3 Human miRNA Microarray. Subsequently, we validated the relative expression of the miRNAs using TaqMan quantitative real-time polymerase chain reaction (RT-qPCR) assays.Serum miRNA-4522, miRNA-324-3p, and miRNA-6767-5p were down-regulated in women with PCOS compared with controls in the microarray analysis. Among these miRNAs, serum miRNA-6767-5p was validated (fold change in women with PCOS/controls = 0.39, P-value<0.05) by RT-qPCR. The miRNA-6767-5p was negatively associated with fasting glucose (? = -0.370) and positively associated with the number of menses per year (? = 0.383) after adjustment for age and BMI (Ps<0.05). Genes targeted by miRNA-6767-5p were involved in the cell cycle and the immune system.Serum miRNA-6767-5p may be a novel candidate as a molecular biomarker in the diagnosis of PCOS and may participate in the development of the metabolic and reproductive traits of PCOS.
| S-EPMC5038950 | biostudies-literature
Project description:Polycystic ovary syndrome (PCOS) is a common reproductive system disease, with hyperandrogenism as the core feature. The pathologies remain to be illustrated. Long noncoding RNAs (lncRNAs) has been proved to be involved in various biological processes of human diseases. However, there were few reports about the research on lncRNAs in PCOS, not to mention hyperandrogenism.
2017-11-10 | GSE106724 | GEO
Project description:To explore the molecular mechanisms of obesity and insulin resistance in the patients with polycystic ovary syndrome (PCOS) at the level of human embryonic stem cells (hESCs).Three PCOS-derived and one non-PCOS-derived hESC lines were induced into adipocytes, and then total mRNA was extracted from these adipocytes. The differential genes between PCOS-derived and non-PCOS-derived adipocytes were identified with GeneChip, and then were validated with real-time PCR.There were 153 differential genes. Of the 153 genes, 91 genes were up-regulated and 62 down-regulated. Nuclear receptor subfamily 0, group B, member 2 (NR0B2) was an up-regulated gene, and GeneChip software system indicated that it was associated with obesity and diabetes. Three PCOS-derived and one non-PCOS-derived hESC lines were induced into adipocytes, and then total mRNA was extracted from these adipocytes. The differential genes between PCOS-derived and non-PCOS-derived adipocytes were identified with GeneChip, and then were validated with real-time PCR.
2013-11-22 | E-GEOD-52422 | biostudies-arrayexpress
Project description:Obesity has been linked with a host of metabolic and reproductive disorders including polycystic ovary syndrome (PCOS). While a distinct link exists between obesity and PCOS, the exact pathogenesis of the disease remains less understood and limited research has explored the impact of diet on the development of PCOS. With the primary symptoms of PCOS including hyperandrogenism, anovulation, and polycystic ovaries, most animal models utilize androgen treatment to effectively induce PCOS. However, these models fail to address the underlying causes of disease symptoms and do not effectively demonstrate the metabolic features of the disease such as hyperinsulinemia. Here, we present a novel rodent model of diet-induced obesity that recapitulates both the metabolic and reproductive phenotypes of human PCOS. In utilizing a high-fat high-sugar (HFHS) diet, we have created a model of PCOS that allows for the study of metabolic parameters and their impact on ovarian follicle development and reproductive health. Animals on the HFHS diet not only demonstrated signs of metabolic impairment, but they also developed polycystic ovaries and experienced irregular estrous cycling marked by an extended period spent in estrus. Though hyperandrogenism was not characteristic of HFHS diet animals as a group, testosterone levels were predictive of a polycystic ovarian morphology. Importantly, PCOS was induced similarly to the disease etiology in humans, allowing this model to offer the unique opportunity to study PCOS at its genesis rather than following the development of disease symptoms.
2017-06-01 | GSE83220 | GEO