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Mol. Hum. Reprod. Advance Access published online on October 14, 2009
Molecular Human Reproduction, doi:10.1093/molehr/gap089
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© The Author 2009. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Demethylation of LHR in dehydroepiandrosterone-induced mouse model of polycystic ovary syndrome

Jia-Qiao Zhu1,2, Liang Zhu3, Xing-Wei Liang1, Fu-Qi Xing3, Heide Schatten4 and Qing-Yuan Sun1,5

1State Key Laboratory of Reproductive Biology, Institute of Zoology, Chinese Academy of Science, Beijing 100101, China. 2College of Veterinary Medicine, Yangzhou University, Jiangsu 225009, China. 3Department of OB/GY, Southern Medical University, Guangzhou 510515, China. 4Department of Veterinary Pathobiology, University of Missouri-Columbia, MO 65211.

5 Corresponding author: Qing-Yuan Sun, Ph.D., Institute of Zoology, Chinese Academy of Sciences, Datun Rd, Chaoyang, Beijing 100101, P. R. China (Fax: +86-10-64807050; E-mail: sunqy{at}ioz.ac.cn)

The cause of polycystic ovary syndrome (PCOS), a complex endocrine disorder, is unknown, but its familial aggregation implies underlying genetic influences. Hyperandrogenemia is regarded as a major endocrine character of the PCOS. In this study, we employed bisulfite sequencing and bisulfite restriction analysis to investigate the DNA methylation status of LHR, AR, FSHR and H19 in dehydroepiandrosterone (DHEA)-induced mouse PCOS model. The results showed that methylation of LHR was lost in ovary from induced PCOS mouse. However, AR, FSHR and H19 had similar methylation pattern in DHEA-treated group and control groups. These data provide evidence for close linkage between DNA demethylation of LHR and PCOS.

Key Words: DNA demethylation/LHR/polycystic ovary syndrome

Submitted on July 24, 2009; resubmitted on October 6, 2009; accepted on October 10, 2009.


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