PRODUCTION OF TRANSFORMING GROWTH-FACTOR-ALPHA BY NORMAL AND POLYCYSTIC OVARIES

Citation
Hd. Mason et al., PRODUCTION OF TRANSFORMING GROWTH-FACTOR-ALPHA BY NORMAL AND POLYCYSTIC OVARIES, The Journal of clinical endocrinology and metabolism, 80(7), 1995, pp. 2053-2056
Citations number
23
Categorie Soggetti
Endocrynology & Metabolism
ISSN journal
0021972X
Volume
80
Issue
7
Year of publication
1995
Pages
2053 - 2056
Database
ISI
SICI code
0021-972X(1995)80:7<2053:POTGBN>2.0.ZU;2-I
Abstract
The mechanism of anovulation in polycystic ovary (PCO) syndrome remain s unknown. As circulating concentrations of FSH are apparently normal, and in vivo granulosa cells from anovulatory PCO are hyperresponsive to FSH, it has been suggested that the ack of follicular development i n anovulatory PCO is caused by overexpression of a paracrine growth fa ctor that inhibits steroidogenesis. Epidermal growth factor and the st ructurally homologous transforming growth factor-alpha (TGF alpha) are suitable candidates for this role, but although the production of the latter has been demonstrated in the ovary, no comparison has been per formed between the levels in normal ovaries and PCO. We compared the l evels of TGF alpha in follicular fluid and in granulosa cell- and thec a-and stroma-conditioned media From normal ovaries and PCO. TGF alpha was present in the range of 0.2-200 ng/mL in follicular fluid. There w as a significant inverse correlation of TGF alpha with follicle size, with no differences between follicles from normal ovaries and PCO. Gra nulosa cell-conditioned medium contained concentrations of TGF alpha r anging from 0.1-200 ng/1000 cells. There was a wide range of concentra tions in theca and stroma-conditioned media, with levels varying from 0.2-100 ng/mg tissue and no consistent effect of LH. There were no sig nificant differences between the levels from normal ovaries or PCO in medium conditioned by any compartment of the ovary. We, conclude that the failure of folliculogenesis in PCO syndrome is not likely to be du e to overproduction of TGF alpha by the ovary.