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¹ INSERM U577-Biomatériaux et Réparation Tissulaire, Université Bordeaux 2 Victor Segalen, Zone Nord, Bâtiment 4A, 2ème étage, 33076 Bordeaux Cedex, France
² Université Victor Segalen Bordeaux 2, Bordeaux, France
³ Molecular Endocrinology Group, Division of Medicine, Faculty of Medicine, MRC Clinical Sciences Centre, Imperial College London, Hammersmith Hospital, Du Cane Road, London W12 0NN, UK
⁴ Laboratoire de Biologie et Ingénierie du Cartilage, Institut de Biologie et Chimie des Protéines, UMR 5086 CNRS/UCBLyon 1, 7 passage du Vercors, 69367 Lyon Cedex 07, France

(Requests for offprints should be addressed to O Chassande; Email: chassande{at}bordeaux.inserm.fr)

The active thyroid hormone, triiodothyronine (T₃), binds to thyroid hormone receptors (TR) and plays an essential role in the control of chondrocyte proliferation and differentiation. Hypo- and hyperthyroidism alter the structure of growth plate cartilage and modify chondrocyte gene expression in vivo, whilst TR mutations or deletions in mice result in altered growth plate architecture. Nevertheless, the particular roles of individual TR isoforms in mediating T₃ action in chondrocytes have not been studied and are difficult to determine in vivo because of complex cellular and molecular interactions that regulate growth plate maturation. Therefore, we studied the effects of TR and TRß on chondrocyte growth and differentiation in primary cultures of neonatal rib chondrocytes isolated from TR- and TRß-deficient mice. T₃ decreased proliferation but accelerated differentiation of rib chondrocytes from wild-type mice. T₃ treatment resulted in similar effects in TR-deficient chondrocytes, but in TRß-deficient chondrocytes, all T₃ responses were abrogated. Furthermore, T₃ increased TRß1 expression in wild-type and TR-deficient chondrocytes. These data indicate that T₃-stimulated differentiation of primary rib chondrocytes in vitro requires TRß and suggest that the TRß1 isoform mediates important T₃ actions in mouse rib chondrocytes.