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Int. J. Mol. Sci. 2017, 18(4), 892; doi:10.3390/ijms18040892

E2/ER β Enhances Calcineurin Protein Degradation and PI3K/Akt/MDM2 Signal Transduction to Inhibit ISO-Induced Myocardial Cell Apoptosis

College of Medicine, China Medical University, Taichung 40402, Taiwan
Department of Emergency Medicine, China Medical University Hospital, Taichung 40402, Taiwan
Department of Biological Science and Technology, China Medical University, Taichung 40402, Taiwan
Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan
Department of Nursing, Meiho University, Pingtung 900, Taiwan
Department of Health and Nutrition Biotechnology, Asia University, Taichung 40402, Taiwan
Department of Hospital and Health Care Administration, Chia Nan University of Pharmacy & Science, Tainan County 700, Taiwan
Department of Surgery, School of Medicine, College of Medicine, Taipei Medical University, Taipei 220, Taiwan
Department of Dermatology, Taipei City Hospital, Renai Branch, Taipei 220, Taiwan
Department of Biotechnology, Bharathiar University, Coimbatore 641 046, India
Graduate Institute of Chinese Medical Science, China Medical University, Taichung 40402, Taiwan
These authors contributed equally to this work.
Author to whom correspondence should be addressed.
Academic Editor: Anthony Lemarié
Received: 6 January 2017 / Revised: 28 March 2017 / Accepted: 11 April 2017 / Published: 24 April 2017
(This article belongs to the Collection Programmed Cell Death and Apoptosis)
View Full-Text   |   Download PDF [2394 KB, uploaded 24 April 2017]   |  


Secretion of multifunctional estrogen and its receptor has been widely considered as the reason for markedly higher frequency of heart disease in men than in women. 17β-Estradiol (E2), for instance, has been reported to prevent development of cardiac apoptosis via activation of estrogen receptors (ERs). In addition, protein phosphatase such as protein phosphatase 1 (PP1) and calcineurin (PP2B) are also involved in cardiac hypertrophy and cell apoptosis signaling. However, the mechanism by which E2/ERβ suppresses apoptosis is not fully understood, and the role of protein phosphatase in E2/ERβ action also needs further investigation. In this study, we observed that E2/ERβ inhibited isoproterenol (ISO)-induced myocardial cell apoptosis, cytochrome c release and downstream apoptotic markers. Moreover, we found that E2/ERβ blocks ISO-induced apoptosis in H9c2 cells through the enhancement of calcineurin protein degradation through PI3K/Akt/MDM2 signaling pathway. Our results suggest that supplementation with estrogen and/or overexpression of estrogen receptor β gene may prove to be effective means to treat stress-induced myocardial damage. View Full-Text
Keywords: 17β-Estradiol; calcineurin; cardiac apoptosis; isoproterenol; apoptosis 17β-Estradiol; calcineurin; cardiac apoptosis; isoproterenol; apoptosis

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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Lin, K.-H.; Kuo, W.-W.; Shibu, M.A.; Day, C.-H.; Hsieh, Y.-L.; Chung, L.-C.; Chen, R.-J.; Wen, S.-Y.; Viswanadha, V.P.; Huang, C.-Y. E2/ER β Enhances Calcineurin Protein Degradation and PI3K/Akt/MDM2 Signal Transduction to Inhibit ISO-Induced Myocardial Cell Apoptosis. Int. J. Mol. Sci. 2017, 18, 892.

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