Estrogens are a group of steroid hormones and they exert significant biological effects on the cardiovascular, musculoskeletal, immune and central nervous system through their interaction with estrogen receptors (ERs), ERα and ERβ. Previous studies reported that estrogen receptor β (ERβ) is localized to mitochondria in various cell lines, whereas little is known about his physiological functions there. Understanding his molecular mechanisms in mitochondria is important, as mitochondria are the

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... ain source of cell energy production and other key processes such as apoptosis. In the present study, we explored the role of mitochondrial ERβ in regulating staurosporine (STS) -induced apoptosis using two stably transfected Neuro-2a murine cell lines. The first cell line is the N2A mtGFPERβ, which overexpresses ERβ as an hybrid protein, with the green fluorescent protein (GFP) with mitochondrial targeting signal (mts) and the second cell line is the N2A mtGFP, which overexpresses GFP, also with mitochondrial targeting signal. Through Western blot analysis in total cell extracts, members of the caspase family (cysteine-aspartic proteases) (Procaspase-9, Caspase-9, Procaspase-3 and Caspase-3) and members of the BCL-2 family (B-cell lymphoma 2, Bcl-2 και BCL2-associated X protein, ΒΑΧ) were studied, in order to assess the role of mtERβ in apoptosis. In the N2A mtGFPERβ cell line, the STS-induced increase of protein levels of Caspase-3 and BAX appears to be reduced after the addition of estradiol (E2), whereas for the N2A mtGFP cell line such effect is not observed. Collectively, the results of this study suggest that in the presence of E2, mitochondrial ERβ has a protective effect against apoptosis in neuronal cells.