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Submitted on August 10, 2006
Accepted on January 16, 2007
Department of Biochemistry, Molecular Biology and Cell Biology; Department of Neurobiology and Physiology; Center for Reproductive Science, Northwestern University, Evanston, IL 60208
* To whom correspondence should be addressed. E-mail: k-mayo{at}northwestern.edu.
In the ovary, the steroid hormone estrogen and the TGF-
superfamily member activin are both produced by granulosa cells and they both have intra-ovarian functions. Emerging evidence has indicated an interaction of these two signaling pathways. Based on the fact that estrogen and activin can impact early follicle formation and development, we hypothesize that estrogen treatment may alter activin signaling in the neonatal ovary. Therefore, this study was designed to examine the effect of neonatal DES and E2 exposure on the mRNA and protein levels of the key factors involved in activin signaling in the mouse ovary. CD-1 mouse pups were given daily injections of diethylstilbestrol (DES), estradiol (E2) or oil on postnatal days 1-5, and ovaries and sera were collected on day 19. Neonatal DES or E2 exposure decreased the number of small antral follicles, induced multi-oocytic follicle (MOF) formation, and decreased activin subunit mRNA and protein levels. Consistent with local loss of subunit expression, the phosphorylation of Smad 2, a marker of activin-dependent signaling, was decreased in the estrogen-treated ovaries. The decreased subunit expression resulted in a decrease in serum inhibin levels, with a corresponding increase in FSH. Estrogen also suppressed activin subunit gene promoter activities, suggesting a direct transcriptional effect. Overall, this study demonstrates that activin subunits are targets of estrogen action in the early mouse ovary.
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