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Am J Physiol Endocrinol Metab (September 17, 2002). doi:10.1152/ajpendo.00226.2002
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Articles in PresS, published online ahead of print September 17, 2002
Am J Physiol Endocrinol Metab, 10.1152/ajpendo.00226.2002
Submitted on May 23, 2002
Accepted on September 7, 2002

Specificity of Thyroid Hormone Receptor Subtype and Steroid Receptor Coactivator (SRC)-1 on Thyroid Hormone Action

Peter M. Sadow1, Olivier Chassande2, Karine Gauthier2, Jacques Samarut2, Jianming Xu3, Bert W. O'Malley3, and Roy E. Weiss4*

1 Department of Medicine, The University of Chicago, Chicago, IL, USA; Department of Pathology, The University of Chicago, Chicago, IL, USA
2 Laboratoire de Biologie Moleculaire et Cellulaire, l'Ecole Normale Superieure de Lyon, Lyon, Lyon, France
3 Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, Tx, USA
4 Department of Medicine, The University of Chicago, Chicago, IL, USA

* To whom correspondence should be addressed. E-mail: rweiss{at}medicine.bsd.uchicago.edu.

Isoforms of the thyroid hormone receptor (TR) {alpha} and TRß genes mediate thyroid hormone action. How TR isoforms modulate tissue-specific thyroid hormone (TH) action remains largely unknown. The steroid receptor coactivator-1 (SRC-1) is among a group of transcriptional coactivator proteins that bind to TRs, along with other members of the nuclear receptor superfamily, and modulates the activity of genes regulated by TH. Mice deficient in SRC-1 possess decreased tissue responsiveness to TH and many steroid hormones; however, it is not known whether or not SRC-1-mediated activation of TH-regulated gene transcription in peripheral tissues, such as heart and liver, is TR isoform specific. We have generated mice deficient in TR{alpha} and SRC-1 (TR{alpha}0/0SRC-1-/-), as well as in TRßand SRC-1 (TRß-/-SRC-1-/-) and investigated thyroid function tests and effects of TH deprivation and TH treatment compared to wild type (WT) mice or those deficient in either TR or SRC-1 alone. The data show that (1) in the absence of TR{alpha} or TRß, SRC-1 is important for normal growth; (2) SRC-1 modulates TR{alpha} and TRß effects on heart rate; (3) two new TRß-dependent markers of TH action in the liver have been identified, osteopontin (up-regulated) and glutathione-S-transferase (down-regulated); and (4) SRC-1 may mediate the hypersensitivity to TH seen in liver of TR{alpha}0/0 mice.




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