Endometrial Transcriptome Changes Following Short-Term Liraglutide Treatment in Infertile Women with PCOS and Obesity
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB77902 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR13385548.fastq.gz | Fastqsanger.gz | |||
| ERR13385549.fastq.gz | Fastqsanger.gz | |||
| ERR13385550.fastq.gz | Fastqsanger.gz | |||
| ERR13385551.fastq.gz | Fastqsanger.gz | |||
| ERR13385552.fastq.gz | Fastqsanger.gz |
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Project description:The aim of the study was to investigate if the use of a 12 weeks liraglutide treatment change the endometrial gene expression during the implantation window in infertile obese women with polycystic ovary syndrome (PCOS) undergoing in-vitro fertilization (IVF). This was a cross-sectional study involving treated and non-treated subjects. Endometrial biop-sies were collected from 20 infertile women with PCOS and BMI ≥30 kg/m2 before the IVF procedure. Endometrium transcriptome of 10 participants who had been pretreated with low-dose liraglutide 1.2 mg QD for 12 weeks and achieved at least a 5% reduction in body weight was compared to endometrium transcriptome of 10 treatment-naive participants who had a sta-ble body weight over the last 12 weeks. Next-generation sequencing was conducted to analyze RNA samples. The resulting data were processed to discern key canonical pathways and pre-dict activations or inhibitions. Gene networks were constructed based on established published associations.
2025-01-01 | E-MTAB-14282 | biostudies-arrayexpress
Project description:Context: Endometrium in polycystic ovary syndrome (PCOS) presents altered gene expression indicating progesterone resistance and predisposing to reduced endometrial receptivity and endometrial cancer. Objective: We hypothesized that an altered endocrine/metabolic environment in PCOS may result in an endometrial M-bM-^@M-^\disease phenotypeM-bM-^@M-^] affecting the gene expression of different endometrial cell populations, including stem cells and their differentiated progeny. Design and setting: A prospective study conducted at an academic medical center. Patients and Main Outcome Measures: Proliferative phase endometrium was obtained from 6 overweight/obese PCOS (NIH criteria) and 6 overweight/obese controls. Microarray analysis was performed on fluorescence-activated cell sorting (FACS)-isolated endometrial epithelial cells (eEP), endothelial cells (eEN), stromal fibroblasts (eSF) and mesenchymal stem cells (eMSC). Gene expression data were validated using microfluidic Q-RT-PCR and immunohistochemistry (IHC). Results: The comparison between eEPPCOS and eEPCtrl showed dysregulation of inflammatory genes and genes with oncogenic potential (CCL2, IL-6, ORM1, TNAIFP6, SFRP4, SPARC). eSFPCOS and eSFCtrl showed upregulation of inflammatory genes (C4A/B, CCL2, ICAM1, TNFAIP3). Similarly, in eMSCPCOS vs. eMSCCtrl the most upregulated genes were related to inflammation and cancer (IL-8, ICAM1, SPRR3, LCN2). IHC scoring showed increased expression of CCL2 in eEPPCOS and eSFPCOS compared to eEPCtrl and eSFCtrl and IL-6 in eEPPCOS compared to eEPCtrl. Conclusions: Isolated endometrial cell populations in women with PCOS showed altered gene expression revealing inflammation and pro-oncogenic changes, independent of BMI, especially in eEPPCOS and eMSCPCOS, compared to controls. The study reveals an endometrial M-bM-^@M-^\disease phenotypeM-bM-^@M-^] in women with PCOS with potential negative effects on endometrial function and long-term health. Proliferative phase endometrium was obtained from 6 overweight/obese PCOS (NIH criteria) and 6 overweight/obese controls. Microarray analysis was performed on fluorescence-activated cell sorting (FACS)-isolated endometrial epithelial cells (eEP), endothelial cells (eEN), stromal fibroblasts (eSF) and mesenchymal stem cells (eMSC). Tissue samples were obtained through the National Institute of Health (NIH)/University of California, San Francisco (UCSF), Human Endometrial Tissue and DNA Bank in accordance with the guidelines of the Declaration of Helsinki. Informed consent was obtained from all participants in the UCSF Center for Reproductive Health, and the study was approved by the UCSF Committee on Human Research. The clinical summary of the study participants is shown in Table 1. Eleven proliferative phase endometrial biopsies (Pipelle, Cooper Surgical Shelton, Connecticut) and one curettage specimen were collected from over-weight (Body Mass Index [BMI, kg/m2] M-bM-^IM-% 27 < 29.9; n=1) and obese (BMI M-bM-^IM-% 30; n=5) women with PCOS (age 30.5M-BM-1 2.1 yrs, BMI 34.13M-BM-1 2.2, NIH criteria (17) and overweight (n=2) and obese (n=4) control women (age 36.50M-BM-11.70 yrs, BMI 35.73M-BM-13.96). All PCOS subjects had normal 17-hydroxyprogesterone, prolactin and thyroid hormone levels. Control samples were obtained from healthy volunteer and women undergoing benign gynecological surgery. All controls reported menstrual cycles with regular interval (25-35 days) and no clinical evidence of having PCOS. Neither PCOS nor control subjects were exposed to hormonal medications for at least 2 months prior to tissue sampling and were confirmed not pregnant.
2013-09-30 | E-GEOD-48301 | biostudies-arrayexpress
Project description:Context: Endometrium in polycystic ovary syndrome (PCOS) presents altered gene expression indicating progesterone resistance and predisposing to reduced endometrial receptivity and endometrial cancer. Objective: We hypothesized that an altered endocrine/metabolic environment in PCOS may result in an endometrial “disease phenotype” affecting the gene expression of different endometrial cell populations, including stem cells and their differentiated progeny. Design and setting: A prospective study conducted at an academic medical center. Patients and Main Outcome Measures: Proliferative phase endometrium was obtained from 6 overweight/obese PCOS (NIH criteria) and 6 overweight/obese controls. Microarray analysis was performed on fluorescence-activated cell sorting (FACS)-isolated endometrial epithelial cells (eEP), endothelial cells (eEN), stromal fibroblasts (eSF) and mesenchymal stem cells (eMSC). Gene expression data were validated using microfluidic Q-RT-PCR and immunohistochemistry (IHC). Results: The comparison between eEPPCOS and eEPCtrl showed dysregulation of inflammatory genes and genes with oncogenic potential (CCL2, IL-6, ORM1, TNAIFP6, SFRP4, SPARC). eSFPCOS and eSFCtrl showed upregulation of inflammatory genes (C4A/B, CCL2, ICAM1, TNFAIP3). Similarly, in eMSCPCOS vs. eMSCCtrl the most upregulated genes were related to inflammation and cancer (IL-8, ICAM1, SPRR3, LCN2). IHC scoring showed increased expression of CCL2 in eEPPCOS and eSFPCOS compared to eEPCtrl and eSFCtrl and IL-6 in eEPPCOS compared to eEPCtrl. Conclusions: Isolated endometrial cell populations in women with PCOS showed altered gene expression revealing inflammation and pro-oncogenic changes, independent of BMI, especially in eEPPCOS and eMSCPCOS, compared to controls. The study reveals an endometrial “disease phenotype” in women with PCOS with potential negative effects on endometrial function and long-term health.
2013-09-30 | GSE48301 | GEO
Project description:Endometrial microbiota in infertile women with and without chronic endometritis
| PRJNA530321 | ENA
Project description:Background: Endometriosis affects approximately 10% of reproductive age women and 30%-50% of infertile women. Decreased endometrial receptivity is mainly responsible for infertile women with minimal/mild endometriosis. Medical therapy to improve fecundity of these women is needed. Metformin is reported to inhibit growth of ectopic lesions in endometriosis, while the effect on eutopic endometrium is unclear. The study was to identify if metformin had effect on eutopic endometrium in women with minimal/mild endometriosis and thus improve their fecundity. Materials and Methods: Paired endometrial tissues of secretory phase from participants with minimal/mild endometriosis were collected before and after two months of metformin treatment and setting metformin-free control. Protein expression profiles of endometrium were analyzed by proteomics. Results: A total of 115 proteins were detected up-regulated after metformin therapy, including Insulin-like growth factor-binding protein 7, α-antitrypsin, apolipoprotein D, Rho GDP-dissociation inhibitor 1, brain form glycogen phosphorylase, and Cathepsin B that associated with endometrial receptivity, while there had no significant changes in controls. These up-regulated markers were validated through target proteomics and further demonstrated with endometriosis mice models. Conclusions: This study revealed that metformin might ameliorate biomarkers expressions of endometrial receptivity in human and mice model. Metformin is potential to improve endometrial receptivity of endometriosis-associated infertility.
2021-07-29 | PXD027648 |
Project description:The goal of the study was to assess transcriptome profile of non-decidualized (non-DE) and decidualized (DE) endometrial stromal cells (eSCs) obtained from women with polycystic ovary syndrome (PCOS, eSCPCOS) and non-PCOS controls (eSCCtrl) in response to short-term estradiol (E2) and/or progesterone (P4) exposure with or without dihydrotestosterone (DHT). The eSCs used for RNA-sequencing (RNA-seq) were isolated from proliferative stage endometrium from women with PCOS (diagnosed based on Rotterdam criteria) and non-PCOS controls (n=6 per group). The same eSCs were used for in vitro validation by immunofluorescence (IF; n=3/group). Tissue validation by immunohistochemistry (IHC) was done using whole biopsy formalin-fixed proliferative (PE) and secretory phase (SE) endometrial samples (IHC; n=6/cycle phase/group). Our data provided the observation that Decidualized eSCPCOS display a distinct transcriptome profile, especially in the presence of DHT.
2021-08-18 | GSE171507 | GEO
Project description:Endometrial microbiota in infertile women receiving in vitro fertilization (IVF)-embryo transfer
| PRJNA547449 | ENA
Project description:Polycystic ovary syndrome (PCOS) is one of the most common endocrinopathies among fertile women. PCOS patients have been confirmed to be accompanied by an increased risk of pregnancy complication, and the exact cause is still unclear. Many factors may cause this situation, and impaired endometrial receptivity could be responsible for adverse pregnancy outcomes in PCOS. Unfortunately, there were still few researches about the molecular mechanisms regarding impaired endometrial receptivity. So we designed this study to explore the secretory endometrial proteome in PCOS patients.
2022-06-09 | PXD024735 | Pride
Project description:We generated scaffold-free endometrial organoids from human primary endometrial tissues. These organoids were subjected to stepwise hormone treatments for 14 days mimicking the proliferative phase of menstrual cycle or with constantly high testosterone mimicking PCOS conditions
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Project description:Why ~70% of women with polycystic ovary syndrome (PCOS) have intrinsic insulin resistance (IR), above and beyond that associated with body mass, including dysfunctional glucose metabolism in adipose tissue (AT), remains a fundamental question. In these experiments, we sought to explore the role of miRNAs in the AT of PCOS and matched controls. Analysis determined that PCOS AT has a differentially expressed miRNA profile, including upregulated miR-93. We observed a significant association between HOMA-IR, and GLUT4 and miR-93 expression in human AT. Our results point to a novel mechanism for regulating insulin-stimulated glucose uptake via miR-93, and demonstrate upregulated miR-93 expression in PCOS, possibly accounting for the IR of the syndrome, and also in non-PCOS women with IR. We performed miRNA microarrays to determine PCOS-related miRNA expression in adipose derived from lean PCOS patients and matched control women. We analyized miRNA from total RNA extracted from subcutaneous (sc) adipose tissue from three lean PCOS patients and three matched control women.
2012-09-06 | E-GEOD-37914 | biostudies-arrayexpress