Project description:Polycystic ovary syndrome (PCOS) is a common gynaecological disorder, characterised by elevated circulating androgens and increased expression of androgen receptor (AR) and by downregulation of Wilms Tumour 1 in the endometrium, The objectives of this study are: 1) Understand the functional role of WT1 in regulating decidualization response in healthy endometrial tissue, and 2) understand how interactions between aberrant WT1 and AR expression in PCOS patients result in dysregulation of deciduallization processes
Project description:Polycystic ovary syndrome (PCOS) is a common endocrine disorder in women resulting in ovulation failure and other metabolic problems. However, the underlying mechanisms of it remain largely uncertain due to its complexity of clinical manifestations. Since PCOS is believed as a systemic disorder involved endocrine, metabolism, immune system and many organs, we therefore want to know what happen in the peripheral blood of patients with PCOS. To this purpose, gene expression patterns of peripheral blood from 10 PCOS patients and 10 healthy women were profiled by microarray. The significance analysis of microarray (SAM) software was employed to screen the differentially expressed genes (DEGs) and gene ontology (GO) was used for functional enrichment analysis. Also, quantitative reverse-transcription PCR (qRT-PCR) was performed to confirm the results from microarray. 181 DEGs with a fold change >2.0 and q-value <0.05 were identified between the groups. Of these genes, 149 were up-regulated and 32 down-regulated in PCOS. Importantly, 14 genes associated with inflammatory response pathway were highly enriched in PCOS. Furthermore, qPCR assays validated the dysregulated inflammatory response genes. Our observation reinforces the hypothesis that PCOS is characterized by the presence of systemic inflammatory changes and inflammation is implicated in the pathogenesis of this entity. Further elucidation of the aberrant expression of inflammation-related genes how to affect the pathogenesis of PCOS may lead to the development of novel preventative and therapeutic strategies.
Project description:The present study consisted in a metabolomic approach in follicular fluid samples from patients with polycystic ovary syndrome and hyper response to in vitro fertilization treatment.
Project description:Polycystic ovary syndrome (PCOS), one of the most common endocrinal diseases among reproductive-aged women,is characterized by hyperandrogenemia, chronic oligo/anovulation and polycystic ovarian morphology. In this research, we presented microarrays to identify the differential expressed protein-coding genes and lncRNAs expression profile in the luteinized granulosa cells obtained from PCOS and healthy control patients.
Project description:Polycystic ovary syndrome (PCOS), one of the most common endocrinal diseases among reproductive-aged women, is characterized by hyperandrogenemia, chronic oligo/anovulation and polycystic ovarian morphology. In this research, we presented microarrays to identify the differential expressed protein-coding genes and lncRNAs expression profile in the endometrium during the window of implantation between the PCOS and healthy subjects.
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.
