Delayed endometrial decidualisation in polycystic ovary syndrome; the role of AR-MAGEA11

Younas, Kinza, Quintela, Marcos, Thomas, Samantha, Garcia-Parra, Jetzabel, Blake, Lauren, Whiteland, Helen, Bunkheila, Adnan, Francis, Lewis W., Margarit, Lavinia, Gonzalez, Deyarina and Conlan, R. Steven 2019. Delayed endometrial decidualisation in polycystic ovary syndrome; the role of AR-MAGEA11. Journal of Molecular Medicine 97 (9) , 1315–1327. 10.1007/s00109-019-01809-6

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Abstract

Polycystic ovary syndrome (PCOS) is a common gynaecological disorder, with a prevalence of up to 12% of women of reproductive age, and is in part characterised by elevated circulating androgens and aberrant expression of androgen receptor (AR) in the endometrium. A high percentage of PCOS patients suffer from infertility, a condition that appears to be linked to mistimed and incomplete decidualisation critically affecting events surrounding embryo implantation. The aim of this study was to examine the involvement of MAGEA11, and the genome-wide role of AR in PCOS. We determined that elevated androgen levels on PCOS cells had an impact on the delayed and incomplete decidual transformation of endometrial cells. The AR co-regulator MAGEA11, a known enhancer of AR function, was constitutively overexpressed throughout the menstrual cycle of PCOS patients, co-localised in the nucleus of PCOS stromal tissue and cells and formed a molecular complex with AR. Genome-wide AR analysis in PCOS stromal cells revealed that AR targets included genes involved in cell death and apoptosis, as well as genes commonly dysregulated in endometrial cancer. Enhanced MAGEA11 and AR-mediated transcriptional regulation may impact on a correct endometrial decidualisation response, subsequently affecting endometrial receptivity in these infertile women.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Biosciences
Publisher:	Springer
ISSN:	0946-2716
Date of Acceptance:	2 June 2019
Last Modified:	17 Sep 2024 12:30
URI:	https://orca.cardiff.ac.uk/id/eprint/172016

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