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(Referência obtida automaticamente do Web of Science, por meio da informação sobre o financiamento pela FAPESP e o número do processo correspondente, incluída na publicação pelos autores.)

T3 rapidly modulates TSH beta mRNA stability and translational rate in the pituitary of hypothyroid rats

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Autor(es):
Goulart-Silva, Francemilson [1] ; de Souza, Paula Bargi [1] ; Nunes, Maria Tereza [1]
Número total de Autores: 3
Afiliação do(s) autor(es):
[1] Univ Sao Paulo, Dept Physiol & Biophys, Inst Biomed Sci, BR-05508900 Sao Paulo - Brazil
Número total de Afiliações: 1
Tipo de documento: Artigo Científico
Fonte: Molecular and Cellular Endocrinology; v. 332, n. 1-2, p. 277-282, JAN 30 2011.
Citações Web of Science: 13
Resumo

Whereas it is well known that T3 inhibits TSH beta gene transcription, its effects on TSH beta mRNA stability and translation have been poorly investigated. This study examined these possibilities, by evaluating the TSH beta transcripts poly(A) tail length, translational rate and binding to cytoskeleton, in pituitaries of thyroidectomized and sham-operated rats treated with T3 or saline, and killed 30 min thereafter. The hypothyroidism induced an increase of TSH beta transcript poly(A) tail, as well as of its content in ribosomes and attachment to cytoskeleton. The hypothyroid rats acutely treated with T3 exhibited a reduction of TSH beta mRNA poly(A) tail length and recruitment to ribosomes, indicating that this treatment decreased the stability and translation rate of TSH beta mRNA. Nevertheless, acute T3 administration to sham-operated rats provoked an increase of TSH beta transcripts binding to ribosomes. These data add new insight to an important role of T3 in rapidly regulating TSH gene expression at posttranscriptional level. (C) 2010 Elsevier Ireland Ltd. All rights reserved. (AU)

Processo FAPESP: 06/61713-0 - Acoes nao genomicas dos hormonios tireoideanos na hipofise de ratos: repercussoes na sintese e secrecao de hormonio do crescimento (gh) e tireotrofico (tsh).
Beneficiário:Maria Tereza Nunes
Modalidade de apoio: Auxílio à Pesquisa - Regular