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Regulation of Type 3 Iodothyronine Deiodinase Expression in Cultured Rat Astrocytes: Role of the Erk Cascade¹

U-488 INSERM-Unité de Recherche Stéroïdes et Système Nerveux (S.P., M.R., J.-M.G., A.-M.L., N.M., M.P., F.C.), 94276 Le Kremlin Bicetre Cedex, France; and the Departments of Medicine and Physiology, Dartmouth Medical School (D.L.S.), Lebanon, New Hampshire 03756

Address all correspondence and requests for reprints to: Dr. Françoise Courtin, U-488 INSERM-Unité de Recherche Stéroïdes et Système Nerveux, 94276 Le Kremlin-Bicêtre Cedex, France.

The type 3 iodothyronine deiodinase (D3) metabolizes thyroid hormones to inactive metabolites in many tissues, including the brain. In the present studies, we have examined the mechanisms by which T₃ (T₃), retinoic acid, 12-O-tetradecanoyl phorbol 13-acetate (TPA), and basic fibroblast growth factor (bFGF) induce D3 expression in primary cultures of neonatal rat astrocytes. In untreated cells, D3 messenger RNA (mRNA) was essentially undetectable by Northern analysis and RT-PCR. However, all four agents induced expression of a 2.4-kb D3 transcript as well as D3 activity. Induction of D3 by TPA and bFGF was more rapid than that by T₃ and retinoic acid, and T₃ potentiated the stimulatory effects of TPA and bFGF. D3 induction by TPA was blocked by GF 109203X, an inhibitor of protein kinase C. In addition, the effects of TPA and bFGF were partially prevented by PD 98059, a specific inhibitor of MEK and the Erk signaling cascade. These studies demonstrate that multiple growth factors and hormones regulate D3 activity in cultured astrocytes by inducing D3 mRNA expression. In addition, the stimulatory effects of TPA and bFGF on D3 mRNA and activity appear to be mediated at least in part by activation of the MEK/Erk signaling cascade.

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