Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/113951
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Type: Journal article
Title: Alternative splicing of the androgen receptor in polycystic ovary syndrome
Author: Wang, F.
Pan, J.
Liu, Y.
Meng, Q.
Lv, P.
Qu, F.
Ding, G.-.L.
Klausen, C.
Leung, P.C.
Chan, H.C.
Yao, W.
Zhou, C.-.Y.
Shi, B.
Zhang, J.
Sheng, J.
Huang, H.
Citation: Proceedings of the National Academy of Sciences of the United States of America, 2015; 112(15):4743-4748
Publisher: National Academy of Sciences
Issue Date: 2015
ISSN: 0027-8424
1091-6490
Statement of
Responsibility: 
Fangfang Wang, Jiexue Pan, Ye Liu, Qing Meng, Pingping Lv, Fan Qu, Guo-Lian Ding, Christian Klausen, Peter C. K. Leung, Hsiao Chang Chan, Weimiao Yao, Cai-Yun Zhou, Biwei Shi, Junyu Zhang, Jianzhong Sheng and Hefeng Huang
Abstract: Polycystic ovary syndrome (PCOS) is one of the most common female endocrine disorders and a leading cause of female subfertility. The mechanism underlying the pathophysiology of PCOS remains to be illustrated. Here, we identify two alternative splice variants (ASVs) of the androgen receptor (AR), insertion and deletion isoforms, in granulosa cells (GCs) in ∼62% of patients with PCOS. AR ASVs are strongly associated with remarkable hyperandrogenism and abnormalities in folliculogenesis, and are absent from all control subjects without PCOS. Alternative splicing dramatically alters genome-wide AR recruitment and androgen-induced expression of genes related to androgen metabolism and folliculogenesis in human GCs. These findings establish alternative splicing of AR in GCs as the major pathogenic mechanism for hyperandrogenism and abnormal folliculogenesis in PCOS.
Keywords: AR; splicing; hyperandrogenism; folliculogenesis; PCOS
Rights: The author(s) retains copyright to individual PNAS articles, and the National Academy of Sciences of the United States of America (NAS) holds copyright to the collective work and retains an exclusive License to Publish these articles, except for open access articles submitted beginning September 2017. For such open access articles, NAS retains a nonexclusive License to Publish, and these articles are distributed under a CC BY-NC-ND license. For volumes 106–114 (2009–September 2017), the author(s) retains copyright to individual articles, and NAS retains an exclusive License to Publish these articles and holds copyright to the collective work.
RMID: 0030089060
DOI: 10.1073/pnas.1418216112
Appears in Collections:Medicine publications

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