| Full text | |
| Author(s): |
Patrícia P. Saraiva
[1]
;
Silvania S. Teixeira
[2]
;
Célia Regina Nogueira
[3]
;
Carlos Roberto Padovani
[4]
Total Authors: 4
|
| Affiliation: | [1] Sao Paulo State University. Botucatu School of Medicine. Department of Medical Clinical - Brasil
[2] Sao Paulo State University. Botucatu School of Medicine. Department of Medical Clinical - Brasil
[3] Sao Paulo State University. Botucatu School of Medicine. Department of Medical Clinical - Brasil
[4] Sao Paulo State University. Botucatu School of Medicine. Department of Biostatistics - Brasil
Total Affiliations: 4
|
| Document type: | Journal article |
| Source: | Arquivos Brasileiros de Endocrinologia e Metabologia; v. 52, n. 1, p. 109-113, 2008-02-00. |
| Abstract | |
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. (AU) | |