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Regular Article |
in the Regulation of Rat Ovarian X-Linked Inhibitor of Apoptosis Protein Expression and Follicular Growth by Follicle-Stimulating Hormone1
a Reproductive Biology Unit and Division of Reproductive Medicine, Department of Obstetrics & Gynecology and Cellular & Molecular Medicine, University of Ottawa,
b Ottawa Health Research Institute, The Ottawa Hospital (Civic Campus), Ottawa, Ontario, Canada K1Y 4E9
c Département de Chimie-Biologie, Université du Québec à Trois-Rivières, Trois-Rivières, Québec, Canada G9A 5H7
The expression of X-linked inhibitor of apoptosis protein (XIAP), a member of a family of intracellular antiapoptotic proteins, is induced by FSH during follicular development in vivo. Whether the XIAP up-regulation by FSH (100 ng/ml) is a direct action of the gonadotropin and is important in the control of granulosa cell proliferation during follicular growth is unclear. The overall objective of the present study was to examine whether the FSH-induced XIAP expression and granulosa cell proliferation during follicular development is mediated by the secretion and action of intraovarian transforming growth factor 
(TGF). In rat follicles cultured for 2 and 4 days, FSH stimulated estradiol production, TGF secretion, XIAP expression, and follicular growth. The theca cells are the primary follicular source of FSH-induced TGF, as indicated by in situ hybridization. Intrafollicular injection of a neutralizing anti-TGF antibody (50–200 ng/ml; immunoglobulin G as control) or addition of estradiol-antagonist ICI 182780 (0.5–100 nM) to the culture media suppressed FSH-induced XIAP expression and follicular growth. The effect of ICI 182780 could be partially reversed by high concentrations of estrogen (250 and 500 nM). Whereas TGF (10–20 ng/ml) significantly increased granulosa cell XIAP content and proliferation in primary granulosa cell cultures, FSH alone was ineffective in eliciting the mitogenic response. Our results support the hypothesis that FSH stimulates granulosa cell proliferation via theca TGF secretion and action in response to increased granulosa cell estradiol synthesis, and that XIAP up-regulation in response to FSH suppresses granulosa cell apoptosis and facilitates FSH-induced follicular growth.
1 Supported by a grant from the Canadian Institutes of Health Research (MOP-10369 to B.K.T.). Y.W. and E.A. were recipients of an NSERC Scholarship and CIHR Fellowship, respectively.
2 Correspondence: Benjamin K. Tsang, Ottawa Health Research Institute, The Ottawa Hospital (Civic Campus), 725 Parkdale Avenue, Ottawa, ON, Canada K1Y 4E9. FAX: 613 761 4403; btsang{at}ohri.ca
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