Activin and transforming growth factor-beta as local regulators of ovarian steroidogenesis in the goldfish.

This study explores the hypothesis that activin and TGFbeta(1) serve as local regulators of ovarian function in the goldfish. Initial studies demonstrated the presence of TGFbeta in the ovary through the use RT-PCR, which amplified a 225 bp product from early vitellogenic (EVIT) and prematurational full-grown (PFG) follicles. This transcript showed high homology to TGFbeta in other teleosts. Both goldfish recombinant activin B and human recombinant TGFbeta(1) suppressed basal testosterone production by EVIT follicles incubated in vitro. Activin B also inhibited hCG-stimulated testosterone production by EVIT follicles. Our experiments suggest that activin B mediates these effects through actions at sites upstream of cholesterol formation and/or mobilization in the steroidogenic pathway, and through mechanisms that were independent of effects on cAMP formation. In experiments with PFG follicles, TGFbeta(1) decreased basal testosterone production. Activin B did not affect T production by PFG follicles, suggesting that this hormone has differential effects on steroidogenesis in the goldfish ovary depending on the stage of ovarian maturity. In other tests with PFG follicles, TGFbeta(1) and activin B, to a limited extent, inhibited the conversion of 17 alpha-OHP to the maturation-inducing hormone, 17 alpha,20 beta-dihydroxy-4-pregnen-3-one. In conclusion, this study shows that TGF is expressed in the goldfish ovary, and that both activin and TGFbeta affect steroid production, which provides evidence that these members of the TGFbeta superfamily may act as local regulators of ovarian function in a teleost.