Journal
MOLECULAR AND CELLULAR ENDOCRINOLOGY
Volume 420, Issue C, Pages 116-124Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.mce.2015.11.027
Keywords
Cardiac muscle; 17 beta-estradiol; Mitochondrial biogenesis; Oxidative stress; GPER
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Funding
- Direccion General de Investigacion y Gestion del Plan Nacional de Investigacion Cientifica, Desarrollo e Innovacion of the Spanish Government [SAF2010-21792]
- Comunitat Autonoma de les Illes Balears [31/2011, AAEE43/2014]
- Balearic Islands Government [FPI11-41523224J, FPI09-43169546H]
- European Social Fund
- FPU grant from the Ministerio de Educacion, Cultura y Deporte of the Spanish Government [AP2012-1004]
- University of Balearic Islands [07-2014-0303240]
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Considering the sexual dimorphism described in cardiac mitochondrial function and oxidative stress, we aimed to investigate the role of 17 beta-estradiol (E-2) in these sex differences and the contribution of E-2 receptors to these effects. As a model of chronic deprivation of ovarian hormones, we used ovariectomized (OVX) rats, half of which were treated with E-2. Ovariectomy decreased markers of cardiac mitochondrial biogenesis and function and also increased oxidative stress, whereas E-2 counteracted these effects. In H9c2 cardiomyocytes we observed that G-protein coupled estrogen receptor (GPER) agonist mimicked the effects of E-2 in enhancing mitochondrial function and biogenesis, whereas GPER inhibitor neutralized them. These data suggest that E-2 enhances mitochondrial function and decreases oxidative stress in cardiac muscle, thus it could be responsible for the sexual dimorphism observed in mitochondrial biogenesis and function in this tissue. These effects seem to be mediated through GPER stimulation. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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