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
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.