Saraiva, Patrícia P. [UNESP]Teixeira, Silvania S. [UNESP]Nogueira, Célia Regina [UNESP]Padovani, Carlos Roberto [UNESP]2022-04-282022-04-282008-01-01Arquivos Brasileiros de Endocrinologia e Metabologia, v. 52, n. 1, p. 109-113, 2008.1677-94870004-2730http://hdl.handle.net/11449/225076Osteoclastogenesis may be regulated via activation of the RANK/RANKL (receptor activator of nuclear factor-kappa B/ receptor activator of nuclear factor-kappa B ligand) system, which Is mediated by osteoblasts. However, the bone loss mechanism induced by T3 (triiodothyronine) is still controversial. In this study, osteoblastic lineage rat cells (ROS 17/2.8) were treated with T3 (10-8M, 10-9M, and 10-10M), and RANKL mRNA (messenger RNA) expression was measured by semiquantitative RT-PCR. Our results show that T3 concentrations used did not significantly enhance RANKL expression compared to controls without hormone treatment. This data suggests that other mechanisms, unrelated to the RANK/RANKL system, might be to activate osteoclast differentiation in these cells. copyright © ABE&M todos os direitos reservados.109-113engBoneRANKLRatROS17/2.8 cellThyroid hormoneArtigo10.1590/S0004-273020080001000152-s2.0-41149119567