Steroidogenic enzyme expression in human corpora lutea in the presence andabsence of exogenous human chorionic gonadotrophin (HCG)

Citation
Wc. Duncan et al., Steroidogenic enzyme expression in human corpora lutea in the presence andabsence of exogenous human chorionic gonadotrophin (HCG), MOL HUM REP, 5(4), 1999, pp. 291-298
Citations number
49
Categorie Soggetti
Cell & Developmental Biology
Journal title
MOLECULAR HUMAN REPRODUCTION
ISSN journal
13609947 → ACNP
Volume
5
Issue
4
Year of publication
1999
Pages
291 - 298
Database
ISI
SICI code
1360-9947(199904)5:4<291:SEEIHC>2.0.ZU;2-X
Abstract
In a human conception cycle, the expected decline in progesterone productio n by the corpus luteum during the late luteal phase is prevented by human c horionic gonadotrophin (HCG) secreted by the implanting blastocyst. This st udy investigated the expression of components of the synthetic pathway for progesterone in human corpora lutea in the presence and absence of HCG in v ivo. Corpora lutea were obtained from: in normally cycling women at the tim e of hysterectomy and classified on the basis of the urinary luteinizing ho rmone (LH) surge as early (n = 3), mid- (n = 3), or late luteal (n = 3); or (ii) women who had received daily doubling doses of HCG (n = 3) to 'rescue ' the corpus luteum. Expression patterns of steroidogenic acute regulatory protein (StAR), cytochrome P450 cholesterol side-chain cleavage (P450(scc)) and 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) were investigated by Northern blotting, in-situ hybridization and immunohistochemistry. Luteal ' rescue' with HCG was associated with the continued expression of these comp onents. In the late luteal phase, in the absence of HCG, expression remaine d but was more variable. The expression of 3 beta-HSD mRNA was significantl y reduced during the luteal phase (P < 0.01). In conclusion, during luteal 'rescue', HCG acts to maintain the steroidogenic pathway. In the absence of HCG, the decline in progesterone production begins in the presence of the main components of the steroidogenic pathway. While unlikely to initiate th is decline, the altered expression levels of these components, particularly that of 3 beta-HSD, may contribute to the continued reduction in progester one production.