Triiodothyronine (T3) does not induce Rankl expression in rat Ros 17/2.8 cells

• Autor(a) principal: Saraiva,Patrícia P.
• Data de Publicação: 2008
• Outros Autores: Teixeira,Silvania S., Nogueira,Célia Regina, Padovani,Carlos Roberto
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Arquivos Brasileiros de Endocrinologia & Metabologia (Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S0004-27302008000100015
• topic: Thyroid hormone; RANKL; Bone; Rat; ROS17/2.8 cell

Osteoclastogenesis 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 (10-8 M, 10-9 M, and 10-10 M), 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.