Endocrinology, Vol 131, 1682-1688, Copyright © 1992 by Endocrine Society

ARTICLES

Induction of type III deiodinase activity in astroglial cells by thyroid hormones

A Esfandiari, F Courtin, AM Lennon, JM Gavaret and M Pierre
U-96 INSERM, Unite de Recherche sur la Glande Thyroide et la Regulation Hormonale, Kremlin-Bicetre, France.

The type III deiodinase (D-III) activity in astroglial cells is induced by multiple pathways activated by cAMP, 12-O-tetradecanoylphorbol-13- acetate (TPA), and fibroblast growth factors (FGFs). This study examines the effects of thyroid hormones on D-III activity in astroglial cells with or without induction by these factors. Addition of 10 nM T3 to the culture medium caused a slow increase in D-III activity, which reached a plateau after 48 h. This increase was concentration dependent (maximal response at 10 nM). Doses as low as 0.3 nM caused significant increases in D-III activity. The effect of T3 was reversible. A dose of 10 nM L-T3, D-T3, T4, 3,5,3'- triiodothyroacetic, or 3'-isopropyl-3,5-diiodothyronine produced 5- to 15-fold increases in D-III activity after 48 h. In contrast, 10 nM L- thyronine, 3-monoiodothyronine, 3,3'-diiodothyronine, 3,5- diiodothyronine, and rT3 were without effect. A dose of 10 nM T3 or T4 amplified the D-III activity stimulated by 0.1 microM TPA, 20 ng/ml acidic FGF, or 1 mM 8-bromo-cAMP 3- to 8-fold. Otherwise, T3 rapidly inhibited D-II activity. This inhibition was concentration dependent, with a half-maximal effect around 10 nM. In conclusion, thyroid hormones induce D-III activity and potentiate the D-III activity induced by cAMP, TPA, and FGFs in astroglial cells. These reversible effects together with inhibition of D-II activity may contribute to protect the brain against hyperthyroidism.

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