Basic fibroblast growth factor (bFGF), insulin like growth factor I and II and transforming growth factor beta (TGF-beta) are assumed to be of importance in the paracrine and autocrine regulation of thyroid growth and function. Using in vitro cultures of isolated intact porcine thyroid follicles, we here present data that support a possible autocrine action of bFGF on proliferation, a possible explanation for the observed potentiation of EGF-stimulated growth by IGF-I, and results on the release and regulation of release of TGF-beta. For growth experiments, thyroid follicles (2 x 10(5) cells) were incubated for 6 days followed by cell counting. For the analysis of EGF binding sites, follicles were preincubated with and without IGF-I (10 ng/mL) for 48 h at 37 degrees C, incubated with 125I-EGF (5 nCi/well) and unlabeled EGF (0.1-500 ng/mL) for 24 h at 4 degrees C (2 x 10(5) cells/well); binding characteristics were calculated from Scatchard analysis. The TGF-beta bioactivity in untreated and acid treated media conditioned with thyroid follicles for 3 days (2 x 10(7) cells) was analyzed with a bioassay using mink lung epithelial cells. Basic FGF (0.1-1 ng/mL) dose-dependently stimulated the proliferation of thyroid follicles up to 135.0 +/- 6.1%; this effect was additive with IGF-I (10 ng/mL) but not with EGF (2 ng/mL). The IGF-I (10 ng/mL) just moderately increased proliferation (128.3 +/- 16%), but potentiated EGF (1 ng/mL)-stimulated growth (from 183.0 +/- 11.0% to 314.0 +/- 3.0%).(ABSTRACT TRUNCATED AT 250 WORDS)