Background: Primary cilia (PC) are conserved structures in the adult thyroid gland of different mammals. We have recently described that, in humans, PC are usually present as a single copy per follicular cell emerging from the follicular cell apex into the follicular lumen. Methods: To better understand the role developed by PC in thyroid hormonogenesis, we investigated their changes in different human functional thyroid diseases (diffuse toxic hyperplasia/ Grave's disease and nodular hyperplasia/nodular goiter), in comparison with normal thyroid tissue, using immunofluorescence, morphometry and electron microscopy analyzes. Results: We found significantly decreased ciliary frequencies in both nodular hyperplasia (51.16±11.69%) and Grave's disease (44.43±23.70%) vs. normal thyroid glands (76.09±7.31%). Similarly, PC lengths were also significantly decreased in both nodular hyperplasia (2.02±0.35 µm) and Grave's disease (2.42±0.48 µm) compared to normal glands (3.93±0.90 µm). Moreover, in Grave's disease patients, hyperactive-follicle foci always showed diminished ciliary frequency and length compared to any other thyroid follicle pattern, independent of their thyroid status. Conclusions: Our results suggest a direct relationship between ciliogenesis and both follicle activity and tissue heterogeneity. Furthermore, the Thyroid
These results clarify the important role of c-erbB-2 proto-oncogene in the pathogenesis of human phaeochromocytoma and confirm the unfavourable prognostic significance of c-erbB-2 expression.
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