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Mitochondria play an important role in 17-estradiol attenuation of H₂O₂-induced rat endothelial cell apoptosis

Center for Surgical Research and Department of Surgery, University of Alabama at Birmingham, Birmingham, Alabama

Submitted 10 August 2006 ; accepted in final form 28 September 2006

Studies have shown salutary effects of 17-estradiol following trauma-hemorrhage on different cell types. 17-Estradiol also induces improved circulation via relaxation of the aorta and has an anti-apoptotic effect on endothelial cells. Because mitochondria play a pivotal role in apoptosis, we hypothesized that 17-estradiol will maintain mitochondrial function and will have protective effects against H₂O₂-induced apoptosis in endothelial cells. Endothelial cells were isolated from rats' aorta and cultured in the presence or absence of H₂O₂, a potent inducer of apoptosis. In additional studies, endothelial cells were pretreated with 17-estradiol. Flow cytometry analysis revealed H₂O₂-induced apoptosis in 80.9% of endothelial cells; however, prior treatment of endothelial cells with 17-estradiol resulted in an 40% reduction in apoptosis. This protective effect of 17-estradiol was abrogated when endothelial cells were cultured in the presence ICI-182780, indicating the involvement of estrogen receptor (ER). Fluorescence microscopy revealed a 17-estradiol-mediated attenuation of H₂O₂-induced mitochondrial condensation. Western blot analysis demonstrated that H₂O₂-induced cytochrome c release from mitochondrion to cytosol and the activation of caspase-9 and -3 were decreased by 17-estradiol. These findings suggest that 17-estradiol attenuated H₂O₂-induced apoptosis via ER-dependent activation of caspase-9 and -3 in rat endothelial cells through mitochondria.

cytochrome c; estrogen receptors; mitochondria