caa a22 4500 60623697X CHVBK 20210128101250.0 cr unu---uuuuu 210128e20150301xx s 000 0 eng 10.1007/s11010-014-2293-y doi (NATIONALLICENCE)springer-10.1007/s11010-014-2293-y Mitochondrial estrogen receptor β inhibits cell apoptosis via interaction with Bad in a ligand-independent manner [Elektronische Daten] [Jiayi Liang, Qiang Xie, Ping Li, Xueyun Zhong, Yunxian Chen] Previous studies reported that estrogen receptor β (ERβ) is localized to mitochondria, whereas little is known about the physiological functions of mitochondrial ERβ. In the present study, we explored the role of mitochondrial ERβ in regulating apoptosis using stable ERβ-expressing and ERβ knockdown cells lines. We found that exogenous ERβ was mainly expressed in mitochondrial but not in nuclear after ERβ overexpression and protected cells from apoptosis induced by hydrogen peroxide (H2O2), ultraviolet (UV), and staurosporine (STS). Moreover, overexpression of ERβ prevented Bax activation, cytochrome c release, caspase-3 activation, and PARP cleavage during apoptosis. Furthermore, knockdown of ERβ significantly suppressed the expression of ERβ in mitochondrial and promoted cell apoptosis induced by H2O2, UV, and STS. Downregulation of ERβ also enhanced Bax activation, cytochrome c release, caspase-3 activation and PARP cleavage. In addition, our study discovered that mitochondrial ERβ interacted with proapoptotic protein Bad in a ligand-independent manner, which suggests that mitochondrial ERβ inhibits Bad, and prevents Bax activation and cytochrome c release. Collectively, the results of this study support that mitochondrial ERβ prevents cell apoptosis via the mitochondrial apoptotic pathway in a ligand-independent manner. Springer Science+Business Media New York, 2014 Mitochondrial nationallicence ERβ nationallicence Apoptosis nationallicence Bad nationallicence Liang Jiayi Department of Hematology, First Affiliated Hospital of Sun Yat-sen University, 510080, Guangzhou, China aut Xie Qiang Department of Pathology, Medical College of Jinan University, 510632, Guangzhou, China aut Li Ping Department of Microsurgery, First Affiliated Hospital of Sun Yat-sen University, 510080, Guangzhou, China aut Zhong Xueyun Department of Pathology, Medical College of Jinan University, 510632, Guangzhou, China aut Chen Yunxian Department of Hematology, First Affiliated Hospital of Sun Yat-sen University, 510080, Guangzhou, China aut Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 401/1-2(2015-03-01), 71-86 0300-8177 401:1-2<71 2015 401 11010 https://doi.org/10.1007/s11010-014-2293-y text/html Onlinezugriff via DOI BK010053 XK010053 XK010000 Metadata rights reserved Springer special CC-BY-NC licence nationallicence 1 research-article jats NATIONALLICENCE NATIONALLICENCE NL-springer NATIONALLICENCE 856 40 https://doi.org/10.1007/s11010-014-2293-y text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Liang Jiayi Department of Hematology, First Affiliated Hospital of Sun Yat-sen University, 510080, Guangzhou, China aut NATIONALLICENCE 700 1- Xie Qiang Department of Pathology, Medical College of Jinan University, 510632, Guangzhou, China aut NATIONALLICENCE 700 1- Li Ping Department of Microsurgery, First Affiliated Hospital of Sun Yat-sen University, 510080, Guangzhou, China aut NATIONALLICENCE 700 1- Zhong Xueyun Department of Pathology, Medical College of Jinan University, 510632, Guangzhou, China aut NATIONALLICENCE 700 1- Chen Yunxian Department of Hematology, First Affiliated Hospital of Sun Yat-sen University, 510080, Guangzhou, China aut NATIONALLICENCE 773 0- Molecular and Cellular Biochemistry Springer US; http://www.springer-ny.com 401/1-2(2015-03-01), 71-86 0300-8177 401:1-2<71 2015 401 11010