The synthesis and actions of steroids and prostaglandins during follicular maturation in the pig.

Abstract

Our understanding of the synthesis and production of follicular steroids and prostaglandins (PG) in the pig is based largely on in-vitro studies with granulosa and theca interna tissues obtained from Graafian follicles at various stages of maturation. As the follicle enlarges before the LH surge, granulosa cells exhibit a decrease in FSH receptors and are less responsive to FSH in terms of cAMP production. Concurrently, there is an increase in granulosa and thecal cell LH receptors associated with an increase in responsiveness to LH and an increase in steroid production. Both granulosa and thecal cells produce oestrogen and progesterone, the rates of production being dependent on the stage of maturation of the follicle and substrate availability. Thecal cells are the principal source of androgens and control oestrogen synthesis by providing aromatizable substrate. After exposure to LH/hCG in vivo, both cell types lose the ability to produce oestrogen in vitro. These studies support the two-cell, two-gonadotrophin hypothesis of ovarian steroidogenesis. In vitro, granulosa and thecal cells exhibit an increased ability to produce PGE-2 and PGF-2 alpha after exposure to LH/hCG in vivo. Follicular PG production appears to be regulated by arachidonic acid availability and PG synthetase activity. In vivo, the follicular fluid concentrations of PGE-2 and PGF-2 alpha increase markedly at the time of ovulation. The increases in PG levels and ovulation can be blocked by indomethacin, an inhibitor of PG synthesis. These studies provide convincing evidence for an intrafollicular source of PGs and are consistent with the hypothesis that LH induces an increase in PG production that is essential for rupture of the follicle. Steroids act on the follicle through autocrine and paracrine mechanisms to modulate follicular growth and differentiation and to regulate steroidogenesis. PG actions on the follicle appear to be exerted via effects on contractile elements of the theca externa, blood vessels and on collagenolytic and other proteolytic enzymes.