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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:The pathological alterations in hearts from polycystic ovary syndrome mice
| PRJNA997915 | ENA
Project description:The pathological alterations in hearts from polycystic ovary syndrome mice [male_PAMH]
| PRJNA997921 | ENA
Project description:The pathological alterations in hearts from polycystic ovary syndrome mice [female_PAMH]
| PRJNA997918 | ENA
Project description:The pathological alterations in hearts from polycystic ovary syndrome mice [NWZ_HFD]
| PRJNA997919 | ENA
Project description:Genetic and epigenetic factors may predispose women to polycystic ovary syndrome (PCOS), a common heritable disorder of unclear etiology. Here we investigated differences in genome-wide gene expression and DNA methylation in adipose tissue from 64 women with PCOS and 30 controls. In total, 1720 unique genes were differentially expressed (Q < 0.05). Six out of twenty selected genes with largest expression difference (CYP1B1, GPT), genes linked to PCOS (RAB5B) or type 2 diabetes (PPARG, SVEP1), and methylation (DMAP1) were replicated in a separate case-control study. In total, 63,213 sites (P < 0.05) and 440 sites (Q < 0.15) were differently methylated. Thirty differentially expressed genes had corresponding changes in 33 different DNA methylation sites. Moreover, a total number of 1913 pairs of differentially expressed "gene-CpG" probes were significantly correlated after correction for multiple testing and corresponded with 349 unique genes. In conclusion, we identified a large number of genes and pathways that are affected in adipose tissue from women with PCOS. We also identified specific DNA methylation pathways that may affect mRNA expression. Together, these novel findings show that women with PCOS have multiple transcriptional and epigenetic changes in adipose tissue that are relevant for development of the disease.
| S-EPMC4791632 | biostudies-literature
Project description:BackgroundEvidence proved the association between gut microbiome dysbiosis and polycystic ovary syndrome (PCOS) in metabolic disorder, decreased fertility, and hyperandrogenism. However, alterations in blood microbiome of PCOS remained unknown.ObjectiveThis study aims to measure the blood microbiome profile of PCOS patients compared with healthy controls by 16S rRNA sequencing and to investigate its association with PCOS.MethodsIn this case-control study, bacterial DNA in blood of 24 PCOS patients and 24 healthy controls was investigated by 16S rRNA gene sequencing using the MiSeq technology. Alpha and beta diversity were used to analyze within-sample biodiversity and similarity of one group to another, respectively. Linear discriminant analysis effect size (LEfSe) was calculated to determine biomarkers between groups. Kyoto Encyclopedia of Genes and Genomes (KEGG) functional prediction was performed at genera level.ResultAlpha diversity of blood microbiome decreased significantly in women with PCOS, and beta diversity analysis demonstrated a major separation between the two groups. In the PCOS group, the relative abundance of Proteobacteria, Firmicutes, and Bacteroidetes decreased significantly, while Actinobacteria increased significantly. Cladogram demonstrated the microbiome differences between the two groups at various phylogenic levels. Meanwhile, linear discriminant analysis (LDA) presented significant decreases in Burkholderiaceae, Lachnospiraceae, Bacteroidaceae, Ruminococcaceae, and S24-7 and significant increases in Nocardioidaceae and Oxalobacteraceae of the PCOS group. KEGG pathway analysis at genera level suggested that 14 pathways had significant differences between the two groups.ConclusionOur findings demonstrated that blood microbiome had a significantly lower alpha diversity, different beta diversity, and significant taxonomic variations in PCOS patients compared with healthy controls.
| S-EPMC8908962 | biostudies-literature
Project description:Polycystic ovary syndrome (PCOS), the most common endocrine disease among premenopausal women, is caused by both genes and environment. We and others previously reported association between single nucleotide polymorphisms (SNPs) in the DENND1A gene and PCOS. We therefore sequenced the DENND1A gene in white patients with PCOS to identify possible alterations that may be implicated in the PCOS pathogenesis. Patients were referred with PCOS and/or hirsutism between 1998 and 2011 (n = 261). PCOS was diagnosed according to the Rotterdam criteria (n = 165). Sequence analysis was performed in 10 patients with PCOS. Additional patients (n = 251) and healthy female controls (n = 248) were included for SNP genotyping. Patients underwent clinical examination including Ferriman-Gallwey score (FG-score), biochemical analyses and transvaginal ultrasound. Mutation analysis was carried out by bidirectional sequencing. SNP genotyping was tested by allelic discrimination in real-time PCR in the additional patients and controls. Sequencing of the DENND1A gene identified eight SNPs; seven were not known to be associated with any diseases. One missense SNP was detected (rs189947178, A/C), potentially altering the structural conformation of the DENND1A protein. SNP genotyping of rs189947178 showed significantly more carriers among patients with PCOS and moderate hirsutism compared to controls. However, due to small sample size and lack of multiple regression analysis supporting an association between rs189947178 and FG-score or PCOS diagnosis, this could be a false positive finding. In conclusion, sequence analysis of the DENND1A gene of patients with PCOS did not identify alterations that alone could be responsible for the PCOS pathogenesis, but a missense SNP (rs189947178) was identified in one patient and significantly more carriers of rs189947178 were found among patients with PCOS and moderate hirsutism vs. controls. Additional studies with independent cohort are needed to confirm this due to the small sample size of this study.
| S-EPMC3785455 | biostudies-literature