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Nucleic Acids Research 2006 34(11):3279-3287; doi:10.1093/nar/gkl387
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Published online 28 June 2006

© 2006 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (
http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commerical use, distribution, and reproduction in any medium, provided the original work is properly cited.


Article

Genes invoked in the ovarian transition to menopause

Alison Zimon1, Anna Erat2, Tiffany Von Wald1, Brad Bissell2, Anna Koulova2, Chu H. Choi2, Dimcho Bachvarov3, Richard H. Reindollar1 and Anny Usheva1,2,*

1 Division of Reproductive Endocrinology and Infertility, Department of Obstetrics and Gynecology, Beth Israel Deaconess Medical Center and Harvard Medical School Boston, MA 02215, USA 2 Division of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School Boston, MA 02215, USA 3 Centre Hospitalier Universitaire de Québec (CHUQ)–Centre de Recherche, Hopital L'Hôtel-Dieu de Québec et Université Laval Québec, Canada G1R 2J6

*To whom correspondence should be addressed. Tel: 11 617 632 0522; Fax: 11 617 6672927; Email: ausheva{at}bidmc.harvard.edu

Received November 27, 2005. Revised January 29, 2006. Accepted May 10, 2006.

Menopause and the associated declines in ovarian function are major health issues for women. Despite the widespread health impact of this process, the molecular mechanisms underlying the aging-specific decline in ovarian function are almost completely unknown. To provide the first gene–protein analysis of the ovarian transition to menopause, we have established and contrasted RNA gene expression profiles and protein localization and content patterns in healthy young and perimenopausal mouse ovaries. We report a clear distinction in specific mRNA and protein levels that are noted prior to molecular evidence of steroidogenic failure. In this model, ovarian reproductive aging displays similarities with chronic inflammation and increased sensitivity to environmental cues. Overall, our results indicate the presence of mouse climacteric genes that are likely to be major players in aging-dependent changes in ovarian function.


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