Mol. Hum. Reprod. Advance Access published online on February 4, 2009
Molecular Human Reproduction, doi:10.1093/molehr/gap006
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Androgen receptor function in mammalian oocytes: a new hypothesis
1State Key Laboratory of Reproductive Biology, Institute of Zoology 2Graduate School, Chinese Academy of Sciences, Beijing, China 3Department of Veterinary Pathobiology, University of Missouri-Columbia, Columbia, Missouri, USA
* Correspondence to: Qing-Yuan Sun; State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Sciences; Datun Road, Chaoyang, Beijing 100101, PR China, Tel.: +8610.6480.7050; Fax: +8610-6480.7050, Email: sunqy{at}ioz.ac.cn or sunqy1{at}yahoo.com
Unlike the well established roles of androgen and androgen receptor (AR) in males, the functions of this steroid and its receptor in the ovary is still unclear. For decades, androgen and AR have long been considered to play a negative (at least not a positive) role in mammalian oocyte maturation. However, recent studies by ourselves and others showed their positive influence in promoting meiotic maturation. On the other hand, rapid non-genomic effects of androgens have been observed and are now generally accepted as contributing to the physiological effects of the steroids and their related receptors in somatic cells, and this has stimulated us to explore the complex roles of AR in the ovary. Based on the classic dogma and new findings, we collected evidence to propose that the expression of AR shifts from the oocytes to the theca cells and finally disappears in the oocytes during evolution.It is suggested that the non-genomic pathway involving androgen and AR in the mammalian, unlike somatic cells will undergo elimination. The function of androgen and AR in promoting meiotic maturation may have been replaced gradually by gonadotrophins. Moreover, a possible relationship between AR and polycystic ovary syndrome (PCOS) is also discussed, which might provide a clue for the pathology of the disease.
This paper was presented at the Beijing International Symposium on Reproductive Biology
Submitted on November 4, 2008; resubmitted on January 7, 2009; accepted on January 20, 2009.