Abstract:
:The predisposition of the testis and ovary to primarily synthesize testosterone (T) and estradiol (E2), respectively, is due to gonadal-specific cell types that differentially express the various hydroxysteroid (17beta) dehydrogenase (HSD17B) isoforms. In testes, Leydig cells rely on LH stimulation to maintain expression of the type 3 (HSD17B3) isoform, which specifically converts androstenedione to T. In ovaries, thecal interstitial (TI) cells also rely on LH to induce androgen synthesis but lack HSD17B3 and therefore secrete androgens of low biological activity. Therefore, thecal cells may possess a mechanism to repress the Leydig cell phenotype and HSD17B3 expression. E2 is known to inhibit experimentally Leydig cell function and proliferation. In the current study, we provide evidence that E2 prevents the development of functional Leydig-like cells in the murine ovary and that this action is mediated by estrogen receptor (ER) alpha. ERalpha-null (alphaERKO) female mice exhibit testis-like levels of Hsd17b3 expression in the ovaries and male-like levels of plasma T. Herein, we demonstrate that: 1) Hsd17b3 expression in alphaERKO ovaries is a primary effect of the loss of intraovarian ERalpha actions; 2) alphaERKO ovarian cells produce substantial levels of T in vitro, and this is blocked by a HSD17B3-specific inhibitor; 3) Hsd17b3 expression in alphaERKO ovaries is LH regulated and localized to the secondary interstitial (SI)/TI cells; and 4) alphaERKO SI/TI cells possess Leydig-like ultrastructural features. These data indicate that intraovarian ERalpha actions are required to repress Hsd17b3 expression in the ovary and may be important to maintaining a female phenotype in SI/TI cells.
journal_name
Endocrinologyjournal_title
Endocrinologyauthors
Couse JF,Yates MM,Rodriguez KF,Johnson JA,Poirier D,Korach KSdoi
10.1210/en.2006-0276subject
Has Abstractpub_date
2006-08-01 00:00:00pages
3666-78issue
8eissn
0013-7227issn
1945-7170pii
en.2006-0276journal_volume
147pub_type
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