IN-VIVO MODULATION OF ANNEXIN-I, ANNEXIN-II AND ANNEXIN-V EXPRESSION BY THYROXINE AND METHYLTHIOURACIL

Regulation of annexin concentration and localization were investigated in thyroid tissues of hypothyroid [methylthiouracil (MeSur) treatment ], euthyroid (control) and hyperthyroid [thyroxine (T4) treatment] rat s. A low level of circulating thyroid hormones induces a decrease of t otal thyroid calcium-binding protein concentration when compared with the concentration in unstimulated animals. Conversely, concentrations of annexins I, II and V increase. The accumulation of these proteins i n two subcellular compartments (cytosolic and particulate fractions) c an be reversed by addition of thyroid hormones. The finding of a speci fic increase in annexins concentration in thyroid-hormone-deficient ra ts, with a general decrease of the total calcium-binding protein conte nt points to a very important role of these proteins in the cells. Fur thermore, hyperthyroidism gives opposite results. To investigate the t ransduction pathway of annexins I-, II- and V-induced biosynthesis by thyroid hormones in thyroid glands, we used cultured pig thyroid cells as in vitro model system. In previous work [16], we have shown that a nnexin concentrations and localization are under TSH control via the a denylate cyclase pathway. In the presence of MeSur (in the culture med ium), the protein-binding iodine remains low, indicative of weak thyro id hormone synthesis (data not shown) and that the annexins content is unchanged. These results suggest that, in thyroid tissue, an indirect mechanism links thyroid hormones to annexin expressions via the TSH f eed-back loop, and excludes autocrine regulation.