Dataset Information

Changes in proteomics of endometrial tissue during secretion of polycystic ovary syndrome may affect endometrial receptivity

ABSTRACT: 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.

INSTRUMENT(S): iTRAQ reagent

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Uterine Endometrium

DISEASE(S): Polycystic Ovary Syndrome

SUBMITTER: Jun Li

LAB HEAD: Zhaolian Wei

PROVIDER: PXD024735 | Pride | 2022-06-09

REPOSITORIES: Pride

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Proteomic alteration of endometrial tissues during secretion in polycystic ovary syndrome may affect endometrial receptivity.

Li Jun J Jiang Xiaohua X Li Caihua C Che Huihui H Ling Lin L Wei Zhaolian Z

Clinical proteomics 20220528 1

Embryo implantation is a complex developmental process that requires coordinated interactions among the embryo, endometrium, and the microenvironment of endometrium factors. Even though the impaired endometrial receptivity of patients with polycystic ovary syndrome (PCOS) is known, understanding of endometrial receptivity is limited. A proteomics study in three patients with PCOS and 3 fertile women was performed to understand the impaired endometrial receptivity in patients with PCOS during lut ...[more]

PMID: 35643455

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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.

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