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Department of Obstetrics and Gynecology (H.W., K.A., L.X., N.K., Y.A., K.Y., R.F.), and First Department of Anatomy (H.H.), Gunma University School of Medicine, Gunma 371-8511; and Department of Obstetrics and Gynecology, Hirosaki University School of Medicine (H.M.), Hirosaki 036-8562, Japan
Address all correspondence and requests for reprints to: Hideki Mizunuma, M.D., Department of Obstetrics and Gynecology, Hirosaki University School of Medicine, 5 Zaifu-cho, Hirosaki, Aomori, 036-8562 Japan. E-mail: mizunuma{at}cc.hirosaki-u.ac.jp
The present study investigates the physiological significance of
dehydroepiandrosterone, dehydroepiandrosterone sulfate, T,
androstenedione (
4), dihydrotestosterone (DHT), estrone
(E1), and E2 on recombinant human FSH- (rhFSH) resistant type 4
follicles obtained from immature mice. Type 4 follicles of a diameter
of 100–120 µm with one or two granulosa cell layers around the
oocyte and an intact basal lamina with theca cells were isolated from
the ovaries of 11-d-old BDF-1 mice and cultured with medium alone
(control) or with dehydroepiandrosterone, dehydroepiandrosterone
sulfate, T, 4, DHT, E1, or E2 at concentrations ranging
from 1 x 10-11 to 1 x 10-7
M for 4 d. We examined the mean diameters of type 4
follicles, levels of immunoreactive (IR)-inhibin, and E2 and
progesterone in the culture media on day 4. In addition, we evaluated
follicular cell proliferation by immunofluorescence staining with
5-bromo-2'-deoxyuridine. All tested androgens significantly increased
the diameter of type 4 follicles in a dose-dependent manner without the
production of IR-inhibin and E2. The nuclei of granulosa cells in type
4 follicles cultured with all tested androgens exhibited intense
5-bromo-2'-deoxyuridine-positive staining, compared with those of
controls. In contrast, neither E1 nor E2 had any stimulatory effects.
The stimulatory effects of T, 4, or DHT were inhibited
by an AR antagonist in a dose-related fashion but not by an aromatase
inhibitor. Furthermore, all tested androgens had a synergistic effect
with rhFSH on follicular growth and the production of IR-inhibin and
E2. These results demonstrated that neither adrenal nor ovarian
androgens are arteriogenic but that they stimulate type 4 follicles
unresponsive to rhFSH and augment the responsiveness of these follicles
to rhFSH.
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