Steroid Receptor Coactivator-1 Deficiency Causes Variable Alterations in the Modulation of T3-Regulated Transcription of Genesin Vivo

We showed that steroid receptor coactivator 1 deficient mice exhibit partial resistance to thyroid hormone at the level of the pituitary thyrotrophs

Yoko Takeuchi; Yoshiharu Murata; Peter Sadow; Yoshitaka Hayashi; Hisao Seo; Jianming Xu; Bert W. O’Malley; Roy E. Weiss; Samuel Refetoff

2014

Scholarcy highlights

  • For this study we examined the expression of two or three T3-responsive genes in each of three target organs: GH and TSH ␤-subunit in pituitary; type 1 iodothyronine 5Ј-deiodinase, spot 14 and malic enzyme in liver; and sarcoplasmic reticulum calcium adenosine triphosphatase 2, myosin heavy chain ␣, and -␤ in heart
  • It is well known that the transcription of TSH␣ and -␤ genes is markedly activated by thyroid hormone deficiency and suppressed by l-T3
  • Hypothyroid SRC-1ϩ/ϩ mice showed an approximately 6-fold increase in S14 mRNA content from thyroid hormone deprivation to l-T3 treatment. These results suggest that down-regulation of S14 mRNA during thyroid hormone deprivation is completely abolished in the steroid receptor coactivator 1 knockout mouse
  • The present study shows that the inactivation of the SRC-1 gene affects T3-mediated modulation of expression of some T3-responsive genes, but not all
  • Expression of GH in the pituitary, of 5ЈDI and ME in liver, as well as any of three T3-responsive genes in heart was not affected by inactivation of the SRC-1 gene in either the thyroid hormone-deprived or rRNA are shown in arbitrary units
  • Some differences in the SRC1-modulated effects may be TR isoform specific, such as the presence or absence of resistance to thyroid hormone on genes negatively regulated through TR␤2 or TR␣1, respectively

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