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Expression of Type 2 Iodothyronine Deiodinase in Corticotropin-Secreting Mouse Pituitary Tumor Cells Is Stimulated by Glucocorticoid and Corticotropin-Releasing Hormone

First Department of Internal Medicine (O.A., T.M., T.O., H.M., M.Mo.) and Department of Laboratory Medicine (M.Mu.), Gunma University School of Medicine, Maebashi 371-8511, Japan

Address all correspondence and requests for reprints to: Masami Murakami, M.D., Department of Laboratory Medicine, Gunma University School of Medicine, Maebashi 371-8511, Japan. E-mail: mmurakam{at}showa.gunma-u.ac.jp.

We identified the presence of iodothyronine deiodinase in AtT-20 mouse pituitary tumor cells that secrete corticotropin. Iodothyronine deiodinating activity in AtT-20 cells fulfills all the characteristics of type 2 iodothyronine deiodinase (D2), including the inhibition by thyroid hormones, the insensitivity to inhibition by 6-propyl-2-thiouracil, and the low Michaelis-Menten constant value for T₄. Northern analysis using mouse D2 cRNA probe demonstrated the hybridization signal of approximately 7.0 kb in size in AtT-20 cells. D2 activity and D2 mRNA were stimulated by glucocorticoid in a dose-dependent manner but were not stimulated by testosterone or ß-estradiol. D2 expression was stimulated by (Bu)2cAMP, and CRH in a dose-dependent manner in the presence of dexamethasone. These results suggest the previously unrecognized role of local thyroid hormone activation by D2 in the regulation of pituitary corticotrophs.

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