Journal
JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 105, Issue 6, Pages 1342-1351Publisher
WILEY
DOI: 10.1002/jcb.21936
Keywords
ESTROGEN; ESTROGEN RECEPTOR; NRF-1; Tfam
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Funding
- NCI NIH HHS [R21 CA124811, R21 CA124811-02] Funding Source: Medline
- NIDDK NIH HHS [R01 DK53220, R01 DK053220, R01 DK053220-10A2] Funding Source: Medline
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Estrogens have cell-specific effects on a variety of physiological endpoints including regulation of mitochondrial biogenesis and activity. Estrogens regulate gene transcription by the classical genomic mechanism of binding to estrogen receptors alpha and beta (ER alpha and ER beta) as well as the more recently described nongenomic pathways involving plasma membrane-associated ERs that activate intracellular protein kinase-mediated phosphorylation signaling cascades. Here I will review the rapid and longer-term effects of estrogen on mitochondrial function. The identification of ER alpha and ER beta within mitochondria of various cells and tissues is discussed with a model of estrogen regulation of the transcription of nuclear respiratory factor-1 (NRF-1, NRF1). NRF-1 subsequently promotes transcription of mitochondrial transcription factor Tfam (mtDNA maintenance factor, also called mtTFA) and then Tfam targets mtDNA-encoded genes. The nuclear effects of estrogens on gene expression directly controlling mitochondrial biogenesis, oxygen consumption, mtDNA transcription, and apoptosis are reviewed. Overall, we are just beginning to evaluate the many direct and indirect effects of estrogens on mitochondrial activities. J. Cell. Biochem. 105: 1342-1351, 2008. (C) 2008 Wiley-Liss, Inc.
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