Thyroid hormones are corequisites for estradiol-17β in vitro induction of Xenopus vitellogenin synthesis and secretion

Abstract

Estradiol-17β administered to male frogs induces liver synthesis and secretion of vitellogenin, the precursor protein of the major egg yolk proteins. Estradiol-17β alone failed to induce this protein in cultures of liver tissue maintained for 1–2 weeks prior to addition of the hormone. If a “complex” defined culture medium, such as Coon's modified Ham's F12 medium, is used, efficient primary and secondary induction of vitellogenin synthesis and secretion occurs in the presence of estradiol-17β, triiodothyronine, and dexamethasone. Using Coon's medium we investigated the role of both triiodothyronine and dexamethasone as corequisites of estradiol-17β induction of secreted vitellogenin. Control cultures given no hormones showed a gradual decrease in the level of secreted albumin and fibrinogen. Addition of dexamethasone, alone, induced increased synthesis of secreted albumin and fibrinogen as well as other proteins. Cultures given thyroid hormones, alone, showed an increased level of secreted albumin and fibrinogen at early time points in the culture period. Thus, at early times thyroid hormones appear to enhance the activity of endogenous glucocorticoids. Independent of their interaction with glucocorticoids, thyroid hormones also enhance the activity of estrogens. Long-term cultures given estradiol-17β, alone, failed to synthesize and secrete vitellogenin. In contrast, cultures given the estrogen together with thyroid hormones showed vitellogenin synthesis. These results imply that similar interactions of several hormones occur in vivo in adult animals treated with estrogens. In the accompanying paper the interaction of dexamethasone with estradiol-17β and triiodothyronine is described (L. J. Wangh, 1982, Develop. Biol. 89, 294–298) .