1,25‐Dihydroxycholecalciferol modulates ³H‐Thymidine Incorporation in FRTL5 Cells

1,25‐dihydroxycholecalciferol (1,25(OH)₂D₃) possesses proliferation and differentiation modulating effects in many cell types in vitro. We studied the effect of 1,25(OH)₂D₃ on ³H‐thymidine incorporation in FRTL5 cells, a cultured rat thyroid follicular cell line. 1,25(OH)₂D₃ alone at 10⁻¹¹ and 10⁻⁹ M exerted no effect on ³H‐thymidine incorporation. However, at 10⁻⁷ M, 1,25(OH)₂D₃ slightly enhanced ³H‐thymidine incorporation. In the presence of 5% calf serum, 1,25(OH)₂D₃ increased ³H‐thymidine incorporation induced by calf serum in a dose‐dependent manner. 1,25(OH)₂D₃ also enhanced ³H‐thymidine incorporation induced by PMA, an extrinsic stimulator of protein kinase C, without directly affecting PMA‐induced protein kinase C translocation. In contrast to the stimulatory effects of 1,25(OH)₂D₃ on the calf serum and PMA‐induced ³H‐thymidine incorporation, 1,25(OH)₂D₃ inhibited the increase in ³H‐thymidine incorporation induced by TSH in a dose‐dependent manner. This effect of 1,25(OH)₂D₃ on TSH‐induced ³H‐thymidine incorporation may be, in part, due to post‐cAMP pathways since 1,25(OH)₂D₃ also inhibited the increase in ³H‐thymidine incorporation induced by Bu₂cAMP without affecting the TSH‐induced increase in cAMP. The stimulatory effect of insulin on ³H‐thymidine incorporation, a cAMP‐independent process, was also inhibited by 1,25(OH)₂D₃. We conclude that 1,25(OH)₂D₃ affects ³H‐thymidine incorporation in FRTL5 cells raising the possibility of a physiologic role for 1,25(OH)₂D₃ in the growth and function of thyroid follicular cells.