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Regulation of androgen receptor expression alters AMPK phosphorylation in the endometrium: In Vivo and In Vitro studies in women with polycystic ovary syndrome

Journal article
Authors Xin Li
Bano Pishdari
P. Cui
Min Hu
H.P. Yang
Y.R. Guo
H.Y. Jiang
Yi Feng
Håkan Billig
Linus Ruijin Shao
Published in International Journal of Biological Sciences
Volume 11
Issue 12
Pages 1376-1389
ISSN 1449-2288
Publication year 2015
Published at Institute of Neuroscience and Physiology, Department of Physiology
Pages 1376-1389
Language en
Links dx.doi.org/10.7150/ijbs.13109
Keywords 5α-dihydrotestosterone , AMPKα , Androgen receptor , Endometrium , PCOS
Subject categories Physiology

Abstract

© 2015 Ivyspring International Publisher. The failure of reproductive success in polycystic ovary syndrome (PCOS) patients could be in part due to endometrial dysfunction. However, no studies have investigated any causality between androgen, androgen receptor (AR) expression, and adenosine monophosphate activated protein kinase (AMPK) activation in the endometrium under physiological and pathological conditions. In the present study, we show that 1) endometrial AR expression levels fluctuate in non-PCOS and PCOS patients during the menstrual cycle; 2) the menstrual phase-dependent alteration of p-AMPKα expression occurs in non-PCOS patients but not in PCOS patients; 3) AR expression is higher in PCOS patients than non-PCOS patients during hyperplasia while AMPKα activation (indicated by the ratio of p-AMPKα to AMPKα); and 4) co-localization of AR and Ki-67 in epithelial cell nuclei is observed in endometrial hyperplasia. Importantly, using in vitro human tissue culture and an in vivo 5α-dihydrotestosterone-treated rat model, we show that the action of androgen on AMPKα activation is likely mediated through nuclear AR, especially in epithelial cells. Collectively, we present evidence that AR expression and AMPKα activation depend on menstrual cycle phase and the presence of PCOS, and the data suggest that AR-mediated regulation of AMPKα activation might play a role in the development of endometrial hyperplasia.

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