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Regulation of Thyroid Cell Proliferation by TSH and Other Factors: A Critical Evaluation of in Vitro Models

Institute of Interdisciplinary Research (IRIBHN) (T.K., A.V.K., J.G., J.E.D., P.P.R.), School of Medicine, Université Libre de Bruxelles, Campus Erasme, B-1070 Brussels, Belgium; and Dipartimento di Biologia e Pathologia Cellulare e Moleculare (A.F.), Facoltà di Medicina e Chirurgia di Napoli, Università degli Studi di Napoli, I-80131 Napoli, Italy

Correspondence: Address all correspondence and requests for reprints to: Dr. J. E. Dumont or Dr. P. Roger at IRIBHN, Faculté de Médecine, Campus Erasme, 808 route de Lennik, B-1070 Bruxelles, Belgium, E-mail: proger@ulb.ac.be and jedumont{at}ulb.ac.be

TSH via cAMP, and various growth factors, in cooperation with insulin or IGF-I stimulate cell cycle progression and proliferation in various thyrocyte culture systems, including rat thyroid cell lines (FRTL-5, WRT, PC Cl3) and primary cultures of rat, dog, sheep and human thyroid. The available data on cell signaling cascades, cell cycle kinetics, and cell cycle-regulatory proteins are thoroughly and critically reviewed in these experimental systems. In most FRTL-5 cells, TSH (cAMP) merely acts as a priming/competence factor amplifying PI3K and MAPK pathway activation and DNA synthesis elicited by insulin/IGF-I. In WRT cells, TSH and insulin/IGF-I can independently activate Ras and PI3K pathways and DNA synthesis. In dog thyroid primary cultures, TSH (cAMP) does not activate Ras and PI3K, and cAMP must be continuously elevated by TSH to directly control the progression through G₁ phase. This effect is exerted, at least in part, via the cAMP-dependent activation of the required cyclin D3, itself synthesized in response to insulin/IGF-I. This and other discrepancies show that the mechanistic logics of cell cycle stimulation by cAMP profoundly diverge in these different in vitro models of the same cell. Therefore, although these different thyrocyte systems constitute interesting models of the wide diversity of possible mechanisms of cAMP-dependent proliferation in various cell types, extrapolation of in vitro mechanistic data to TSH-dependent goitrogenesis in man can only be accepted in the cases where independent validation is provided.

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