OR08-2 Androgen Receptor- Vs Estrogen Receptor-Mediated Actions in the Development of Distinct Clinical Polycystic Ovary Syndrome (PCOS) Phenotypes

Abstract Context: Recent evidence indicates that the increase in follicle numbers seen in polycystic ovary syndrome occurs early in folliculogenesis, with androgens being a likely causative candidate. In primates and sheep, androgen excess in utero results in ovarian changes similar to those in polycystic ovary syndrome. There is also increasing interest in the role of anti-Müllerian hormone (AMH) in early folliculogenesis because AMH knockout mice have an early depletion of their stock of primordial follicles. Initiation and early folliculogenesis may therefore be under negative control by AMH and positive control by androgens. Objective: Because AMH signals exclusively through its type II receptor (AMHRII), the aim of this study was to determine and colocalize the stage-specific expression of AMHRII, androgen receptor (AR), and FSH receptor (FSHR) mRNA in individual, well-characterized preantral follicles. Method: Follicles were isolated from human ovarian cortex obtained from either oophorectomies or cortical biopsies at cesarean section. Expression of AR, FSHR, and AMHRII mRNA was determined using a nested RT-PCR protocol. Results: AR mRNA was not detected in any primordial follicles but was from the transitional stage onward. The number of AR-positive follicles increased at each progressive growth stage. The expression of AR preceded that of FSHR, and only a small percentage of primary follicles expressed FSHR. AMHRII expression was rarely detected. Conclusions: This is the first study to identify the expression of AR in human transitional follicles. Results suggest a role for androgens in promoting early follicle growth and challenging the hypothesis that AMH exerts a direct, inhibitory effect on follicles at this stage.

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Systematic review of cell adhesion molecules and estrogen receptor expression in the endometrium of patients with polycystic ovary syndrome

International Journal of Gynecology & Obstetrics ◽

10.1016/j.ijgo.2014.10.022 ◽

2014 ◽

Vol 129 (1) ◽

pp. 1-4 ◽

Cited By ~ 16

Author(s):

Maria Cândida P. Baracat ◽

Paulo C. Serafini ◽

Ricardo dos S. Simões ◽

Gustavo A.R. Maciel ◽

José M. Soares ◽

...

Keyword(s):

Systematic Review ◽

Estrogen Receptor ◽

Cell Adhesion ◽

Polycystic Ovary Syndrome ◽

Adhesion Molecules ◽

Cell Adhesion Molecules ◽

Polycystic Ovary ◽

Receptor Expression ◽

Estrogen Receptor Expression ◽

Ovary Syndrome

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EL-001 Rs6152G/a polymorphism of androgen receptor gene and polycystic ovary syndrome

Reproductive BioMedicine Online ◽

10.1016/s1472-6483(10)61567-2 ◽

2008 ◽

Vol 16 ◽

pp. S-40-S-41

Author(s):

CY Peng ◽

XY Long ◽

GX Lu

Keyword(s):

Androgen Receptor ◽

Polycystic Ovary Syndrome ◽

Polycystic Ovary ◽

Receptor Gene ◽

Androgen Receptor Gene ◽

Ovary Syndrome

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Association of Estrogen Receptor Genes Polymorphisms With Polycystic Ovary Syndrome: A Systematic Review and Meta-Analysis Based on Observational Studies

Frontiers in Endocrinology ◽

10.3389/fendo.2021.726184 ◽

2021 ◽

Vol 12 ◽

Author(s):

Siyu Zhou ◽

Shu Wen ◽

Yongcheng Sheng ◽

Meina Yang ◽

Xiaoyang Shen ◽

...

Keyword(s):

Systematic Review ◽

Estrogen Receptor ◽

Polycystic Ovary Syndrome ◽

Publication Bias ◽

Polycystic Ovary ◽

Meta Analysis ◽

Genetic Models ◽

Cochrane Library ◽

Ovary Syndrome ◽

Subgroup Analyses

PurposeControversial results existed in amounts of studies investigating the authentic association of estrogen receptor genes (ESR1 and ESR2) polymorphisms with the occurrence and progression of polycystic ovary syndrome (PCOS). The inconsistency might result from different loci, sample sizes, and ethnicities. To find the potential correlations between ESR1/ESR2 polymorphisms and PCOS risk, we conducted the first systematic review and meta-analysis to comprehensively summarize current studies in a large combined population.MethodsEligible studies were retrieved from PubMed, MEDLINE, EMBASE, Cochrane Library, CBM, CNKI, WANFANG, and VIP up to February 28, 2021. The quality of studies was assessed using the Newcastle–Ottawa Scale (NOS) scoring system. Odds ratios (ORs) and 95% confidence intervals (95%CIs) were calculated to synthesize data in five genetic models. Subgroup analyses were conducted by ethnicity. Heterogeneity and publication bias were also assessed. The protocol was registered in PROSPERO under the number CRD42021239200.ResultsA total of 8 studies involving 1,522 PCOS patients and 4,198 controls were included. No evidence demonstrated the association of ESR1 rs2234693 (OR=1.07 95%CI 0.98–1.18), ESR1 rs9340799 (OR=0.99 95%CI 0.69–1.43), or ESR2 rs4986938 (OR=1.06 95%CI 0.81–1.38) polymorphisms and PCOS risk in five genetic models. According to stratified subgroup analyses, ethnicity was considered the major source of heterogeneity. No publication bias was found in eligible studies.ConclusionThe present meta-analysis found no significant associations between the variants of ESR1 rs2234693, ESR1 rs9340799, ESR2 rs4936938, and individual PCOS susceptibility, even if ethnicity was taken into account.Systematic Review RegistrationThe protocol was registered in PROSPERO (available from https://www.crd.york.ac.uk/PROSPERO) with the ID number CRD42021239200.

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