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OBJECTIVE: To investigate the expression of thymosin beta10 - a small conserved acidic protein involved in the inhibition of actin polymerization - in human and experimental thyroid goiters as well as the regulation exerted by TSH on thymosin beta10 expression in thyroid follicular cells both in vivo and in vitro. DESIGN: To this aim, we have used 5 bioptic specimens from patients affected by thyroid goiter, a well known experimental model of thyroid goitrogenesis (rat fed with the drug propylthiouracil) and a cultured rat thyroid cell line (PC Cl 3 cells) as a model system. RESULTS: We report that the mRNA expression of thymosin beta10 is markedly enhanced in human goiters compared with normal thyroid. In vivo results showed that the steady-state level of thymosin beta10 mRNA is up-regulated in the thyroid gland of propylthiouracil-fed rats in parallel with follicular cell proliferation: iodide administration to goitrous rats, which induced a marked involution of thyroid hyperplasia, reduced the mRNA level of thymosin beta10. Finally, in vitro studies showed that in cultured rat thyrocytes, the expression of thymosin beta10 mRNA is induced in a time- and dose-dependent manner by the activation of pathways which are mitogenic for thyroid cells (i.e. the protein kinase (PK) A and PKC pathways). CONCLUSION: Taken together, the findings reported here demonstrate that thymosin beta10 expression is regulated by extracellular signals that stimulate growth of thyroid cells both in vitro and in vivo, and suggest a role for this protein in thyroid diseases characterized by proliferation of follicular cells.

The production of thyroglobulin (TG) by cultured rat thyroid cells was demonstrated at the level of a single cell using a modified reverse plaque-forming assay. Thyroid cells were cultured in the presence of sheep erythrocytes (SE) coated with hybrid antibody specific for both SE and TG. Upon the addition of anti-TG serum and complement, hemolytic plaques appeared around TG-producing cells. The kinetics of plaque formation and the distribution of plaque dimensions were investigated. The number of plaqueforming cells reached a peak after 48–72 h of culture, and at this time, 40–60% of the cells were producing TG; the number of plaque-forming cells declined thereafter, reaching a plateau after 5–7 days of culture. This behavior could be related to changes in TG production during the cell cycle. Most plaques showed a single thyroid cell in the center, thus suggesting that, at least in vitro, follicular organization is not an absolute requirement for TG secretion.