Hypothyroidism and hyperthyroidism modulates Ras-MAPK intracellular pathway in rat thyroids.
Endocrine
; 31(2): 174-8, 2007 Apr.
Article
em En
| MEDLINE
| ID: mdl-17873330
Thyrotrophin induces proliferation and function in thyroid cells acting through a seven transmembrane G protein-coupled receptor. The proliferative pathways induced by thyrotropin (TSH) in thyrocytes in vivo are not completely understood yet. The aim of this work is to evaluate if Ras can be induced by TSH in rat thyroids, and whether extracellular regulated kinase (ERK) may be involved in the subsequent intracellular signalling cascade. We induced hypothyroidism in Wistar rats by methimazole (MMI) treatment (0.03% in the drinking water for 21 days). A subset of the hypothyroid rats received T4 (1 microg/100 g bw) during the last 10 days of MMI treatment. Hyperthyroidism was induced by subcutaneous injections of T4 (10 microg/100 g bw) during 10 days in another group of rats. Our data show that in the hypothyroid rats there is a clear positive Ras modulation, but a decrease in pERK. In contrast, thyroidal pERK increases in T4-induced hyperthyroidism, but without any change in RAS, although these changes did not reach statistical significance. Thus, while the rat thyroid proliferation induced by TSH may involve an increase in RAS signalling, the subsequent cascade does not involve ERK phosphorilation, which in fact, increases during T4-induced hyperthyroidism.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Glândula Tireoide
/
Proteínas ras
/
Sistema de Sinalização das MAP Quinases
/
Hipertireoidismo
/
Hipotireoidismo
Limite:
Animals
Idioma:
En
Revista:
Endocrine
Assunto da revista:
ENDOCRINOLOGIA
Ano de publicação:
2007
Tipo de documento:
Article
País de afiliação:
Brasil
País de publicação:
Estados Unidos