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Dexamethasone represses 3,5,3'-triiodothyronine-stimulated expression of intercellular adhesion molecule-1 in the
J B Dietrich1, M Zaepfel, S Kuchler-Bopp
1Laboratoire de Neurobiologie Moléculaire des Interactions Cellulaires, CNRS, Strasbourg, France. jbdietrich@neurochem.u-strasbg.fr
Abstract:
The effect of the thyroid hormone L-3,5,3'-triiodothyronine (T3) on the expression of ICAM-1, a cell surface glycoprotein playing a pivotal role in inflammatory responses, was investigated. In ECV 304 cells, T3 (30 nmol/L) markedly increased ICAM-1 protein expression, with a peak after 24 h of treatment. ECV 304 human cells express both alpha1 and beta1 T3 receptors. In an attempt to understand the molecular mechanisms leading to the induction of the ICAM-1 gene by T3, we have studied the effects of a synthetic glucocorticoid, dexamethasone, and of a sesquiterpene lactone, parthenolide, on this T3-stimulated expression of ICAM-1. Our results demonstrate a repressive effect of dexamethasone and parthenolide on the expression of the protein ICAM-1 stimulated by T3. Both anti-inflammatory compounds interfere with this T3-mediated pathway in a dose-dependent manner.