Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 290, Issue 1-2, Pages 51-59Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2008.04.013
Keywords
mitochondria; estrogen; estradiol; estrogen receptor beta; apoptosis; neurodegeneration; neuroprotection
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Funding
- NIA NIH HHS [P01 AG010485, P01 AG022550, P01 AG027956] Funding Source: Medline
- NINDS NIH HHS [R01 NS054687, R01 NS054651, R01 NS054687-01A2, R01 NS054651-01A2] Funding Source: Medline
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Estrogens are potent neuroprotective hormones and mitochondria are the site of cellular life-death decisions. As such, it is not surprising that we and others have shown that estrogens have remarkable effects on mitochondrial function. Herein we provide evidence for a primary effect of estrogens on mitochondrial function, achieved in part by the import of estrogen receptor beta (ER beta) into the mitochondria where it mediates a number of estrogen actions on this vital organelle. ER beta is imported into the mitochondria, through tethering to cytosolic chaperone protein and/or through direct interaction with mitochondrial import proteins. in the mitochondria, ER beta can affect transcription of critical mitochondrial genes through the interaction with estrogen response elements (ERE) or through protein-protein interactions with mitochondrially imported transcription factors. The potent effects of estrogens on mitochondrial function, particularly during mitochondrial stress, argues fora role of estrogens in the treatment of mitochondrial defects in chronic neurodegenerative diseases like Alzheimer's disease (AD) and Parkinson's disease (PD) and more acute conditions of mitochondrial compromise, like cerebral ischemia and traumatic brain injury. (C) 2008 Published by Elsevier Ireland Ltd.
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