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This Article Full Text Full Text (PDF) All Versions of this Article: 68/5/1911    most recent biolreprod.102.011494v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Zachos, N. C. Articles by Pepe, G. J. Search for Related Content PubMed PubMed Citation Articles by Zachos, N. C. Articles by Pepe, G. J. Agricola Articles by Zachos, N. C. Articles by Pepe, G. J.

Developmental Regulation of Follicle-Stimulating Hormone Receptor Messenger RNA Expression in the Baboon Fetal Ovary¹

Department of Physiological Sciences,³ Eastern Virginia Medical School, Norfolk, Virginia 23501 Departments of Obstetrics/Gynecology/Reproductive Sciences and Physiology,⁴ Center for Studies in Reproduction, University of Maryland School of Medicine, Baltimore, Maryland 21201

In the adult ovary, pituitary FSH via interaction with its receptor (FSHR) is required for follicular maturation and granulosa cell development. In humans and nonhuman primates, the pool of follicles available for adult ovarian function is established in utero. However, our understanding of the ontogeny and developmental regulation of FSHR in the ovary of the primate fetus is incomplete. Our goal was to determine whether the baboon fetal ovary expresses the full-length FSHR mRNA transcript and whether levels are developmentally regulated. Fetal ovaries were obtained at mid (Day 100) and late (Day 165) gestation (term = Day 184) from untreated baboons and on Day 165 from baboons in which fetal estrogen levels were either decreased by >95% by treatment with the aromatase inhibitor CGS 20267 or restored to 30% of normal by treatment with CGS 20267 plus estradiol benzoate administered s.c. to the mother on Days 100–164. The full-length 2088-base pair FSHR mRNA transcript was expressed in ovaries of adult and fetal baboons untreated or treated with CGS 20267 or CGS 20267 and estrogen. Mean (±SEM) FSHR mRNA levels (ratio of FSHR mRNA:18S rRNA), quantified by reverse transcription polymerase chain reaction, were increased (P < 0.05) 2-fold between mid (0.34 ± 0.06) and late gestation (0.76 ± 0.07), an increase prevented (P < 0.05) in estrogen-depleted baboons (0.44 ± 0.10) and partially restored by treatment with CGS 20267 and estrogen (0.58 ± 0.16). We previously showed that the number of follicles/0.33 mm² in fetal ovaries of untreated baboons in late gestation was reduced 50% by treatment with CGS 20267 and restored to normal in baboons treated with CGS 20267 and estrogen. Thus, when corrected for the number of follicles/0.33 mm², FSHR mRNA levels were similar in baboon fetal ovaries untreated (0.010 ± 0.001) or treated with CGS 20267 (0.009 ± 0.002) or CGS 20267 and estrogen (0.007 ± 0.003). We conclude that estrogen plays a major role in regulating ovarian FSHR mRNA expression in the primate fetus, and that the developmental increase in FSHR mRNA levels reflects the estrogen-dependent increase in folliculogenesis (i.e., increased number of granulosa cells and oocytes).

¹ This work was supported by NIH grant U54 HD 36207 as part of the NICHD Specialized Cooperative Centers Program in Reproduction Research.

² Correspondence: Gerald J. Pepe, Department of Physiological Sciences, Eastern Virginia Medical School, P.O. Box 1980, Norfolk, VA 23501-1980. FAX: 757 624 2269; pepegj{at}evms.edu

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