INVESTIGADORES
ORTEGA Hugo Hector
artículos
Título:
Ovarian expression of 11β-Hydroxysteroid Dehydrogenase (11βHSD): Effects of ACTH and its relation with bovine cystic ovarian disease
Autor/es:
AMWEG A; SALVETTI NR; STANGAFERRO M; PAREDES A; LARA HE; RODRIGUEZ F; ORTEGA HH
Revista:
DOMESTIC ANIMAL ENDOCRINOLOGY
Editorial:
ELSEVIER SCIENCE INC
Referencias:
Lugar: Amsterdam; Año: 2013 vol. 45 p. 126 - 140
ISSN:
0739-7240
Resumen:
Cystic ovarian disease (COD) is an important cause of infertility in cattle, and ACTH hasbeen involved in regulatory mechanisms related to ovarian function associated withovulation, steroidogenesis, and luteal function. Here, we examined the localization of 11bhydroxysteroiddehydrogenase type 1 (11bHSD1) and 11bHSD2 proteins in the ovary ofhealthy cows and animals with spontaneous and ACTH-induced COD and the in vitroresponse of the follicular wall exposed to ACTH. After stimulation by ACTH, we documentedchanges in 11bHSD expression and cortisol secretion by the follicular wall of largeantral and follicular cysts. Follicular cysts showed a higher constitutive expression of bothenzymes, whereas ACTH induced an increase in 11bHSD1 in tertiary follicles and follicularcysts and a decrease in 11bHSD2 in follicular cysts. Moderate expression of 11bHSD1 wasobserved by immunohistochemistry in granulosa of control animals, with an increase (P <0.05) from primary to secondary, tertiary, and atretic follicles. The level of immunostainingin theca interna was lower than that in granulosa. The expression of 11bHSD2 was lower inthe granulosa of primary follicles than in that of secondary, tertiary, and atretic folliclesand was lower in the theca interna than in the granulosa. In ACTH-induced and spontaneouslyoccurring follicular cysts, differences from controls were observed only in theexpression of 11bHSD1 in the granulosa, being higher (P < 0.05) than in tertiary follicles.These findings indicate that follicular cysts may be exposed to high local concentrations ofactive glucocorticoids and indicate a local role for cortisol in COD pathogenesis and inregulatory mechanisms of ovarian function.