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Mol. Hum. Reprod. Advance Access published online on August 1, 2006
Molecular Human Reproduction, doi:10.1093/molehr/gal065
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© The Author 2006. 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
Received May 17, 2006
Revised June 6, 2006
Accepted June 21, 2006

Article

Expression of endometrial glycogen synthase kinase-3{beta} protein throughout the menstrual cycle and its regulation by progesterone

Wael Salameh 1, Jason P. Helliwell 2, Guang Han 2, Laron McPhaul 3, and Omid Khorram 2 *

1 Department of Internal Medicine; Present address: Quest Diagnostics, San Juan Capistrano, CA, USA
2 Department of Obstetrics and Gynecology, Harbor-UCLA Medical Center, Torrance, CA, USA
3 Department of Pathology, Harbor-UCLA Medical Center, Torrance, CA, USA

* To whom correspondence should be addressed.
Omid Khorram, E-mail: okhorram{at}obgyn.humc.edu


  Abstract

Glycogen synthase kinase-3{beta} (GSK-3{beta}) is a serine/threonine kinase that plays a role in glycogen synthesis by inhibiting glycogen synthase (GS) through phosphorylation. We hypothesized that GSK-3{beta} by virtue of its role in glycogen synthesis through the inhibition of GS will play a role in the preparation of the endometrium for blastocyst implantation. Immunohistochemical (IHC) analysis and Western blot analysis (WBA) detected GSK-3{beta} in the endometrium, myometrium, Fallopian tube and ovary. WBA showed more than 5-fold higher endometrial expression of the phosphorylated GSK-3{beta} (pGSK-3{beta}) isoform (inactive) in the secretory phase as compared with the proliferative phase (P < 0.001), whereas no differences in total GSK-3{beta} expression were detected. IHC analysis confirmed the WBA and showed marked expression of pGSK-3{beta} predominantly in glandular epithelial cells in early and mid secretory endometrium with scant expression during the proliferative phase. In in vitro experiments using human endometrial-derived epithelial cell line (HES), progesterone did not alter total GSK mRNA or protein expression. However, pro-gesterone induced a dose-dependent increase in the expression of pGSK-3{beta}, which could be blocked by RU486. Cyclic expression of GSK-3{beta}’s active and inactive forms in the endometrium suggests that sex hormones regulate the expression of this enzyme. In vitro experiments demonstrate that progesterone through receptor-mediated mechanisms induces phosphorylation of endome-trial GSK-3{beta}.

Keywords: endometrium/glycogen synthase kinase-3{beta}/menstrual cycle/progesterone/RU486.
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