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Regulation of mitochondrial biogenesis by thyroid hormone

Published online by Cambridge University Press:  28 January 2003

Joachim M. Weitzel ,
K. Alexander H. Iwen  and
Hans J. Seitz
Joachim M. Weitzel
Affiliation:
Institut für Medizinische Biochemie und Molekularbiologie, Abteilung für Biochemische Endokrinologie, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany
K. Alexander H. Iwen
Affiliation:
Institut für Medizinische Biochemie und Molekularbiologie, Abteilung für Biochemische Endokrinologie, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany
Hans J. Seitz
Affiliation:
Institut für Medizinische Biochemie und Molekularbiologie, Abteilung für Biochemische Endokrinologie, Universitätsklinikum Hamburg-Eppendorf, Hamburg, Germany
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Abstract

Thyroid hormone (T3) has a profound effect on mitochondrial biogenesis. T3-regulated gene expression is mediated by thyroid hormone receptor (TR) binding to thyroid hormone response elements (TREs). In concert with the action of various coactivators and corepressors this interaction leads to a modulation of the chromatin structure and subsequently to a modulation of gene expression of adjacent target genes. However, as numerous genes are endogenous regulated by T3 whereas a TRE appears to be absent in their regulatory elements, a TR-independent pathway of T3-mediated gene regulation is likely. In this review, we discuss the direct mechanisms of TR-dependent regulation of gene expression on the nuclear and mitochondrial genome by T3. We also summarise recent observations on an indirect mechanism of T3 action via intermediate factor(s). We discuss the regulation of nuclear respiratory factor 1 (NRF-1) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) by T3, suggesting NRF-1 and PGC-1α as attractive candidate factors for an intermediate factor of T3 action in vivo. Experimental Physiology (2003) 88.1, 121-128.

Thyroid hormone (T3) has a profound effect on mitochondrial biogenesis. T3-regulated gene expression is mediated by thyroid hormone receptor (TR) binding to thyroid hormone response elements (TREs). In concert with the action of various coactivators and corepressors this interaction leads to a modulation of the chromatin structure and subsequently to a modulation of gene expression of adjacent target genes. However, as numerous genes are endogenously regulated by T3, and a TRE appears to be absent in their regulatory elements, a TR-independent pathway of T3-mediated gene regulation is likely. In this review, we discuss the direct mechanisms of TR-dependent regulation of gene expression on the nuclear and mitochondrial genome by T3. We also summarise recent observations on an indirect mechanism of T3 action via intermediate factor(s). We discuss the regulation of nuclear respiratory factor 1 (NRF-1) and peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PGC-1α) by T3, suggesting NRF-1 and PGC-1α as attractive candidates for an intermediate factor of T3 action in vivo.

Type
Special Review Series - Biogenesis and Physiological Adaptation of Mitochondria
Information
Experimental Physiology , Volume 88 , Issue 1 , January 2003 , pp. 121 - 128
Copyright
© The Physiological Society 2003

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