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Title: | E2/ER beta Enhances Calcineurin Protein Degradation and PI3K/Akt/MDM2 Signal Transduction to Inhibit ISO-Induced Myocardial Cell Apoptosis |
Authors: | Lin, Kuan-Ho Kuo, Wei-Wen Shibu, Marthandam Asokan Day, Cecilia-Hsuan Hsieh, You-Liang Chung, Li-Chin Chen, Ray-Jade Wen, Su-Ying Viswanadha, Vijaya Padma Huang, Chih-Yang |
Contributors: | China Med Univ, Coll Med China Med Univ Hosp, Dept Emergency Med China Med Univ, Dept Biol Sci & Technol China Med Univ, Grad Inst Basic Med Sci Meiho Univ, Dept Nursing Asia Univ, Dept Hlth & Nutr Biotechnol Chia Nan Univ Pharm & Sci, Dept Hosp & Hlth Care Adm Taipei Med Univ, Coll Med, Sch Med Taipei City Hosp, Renai Branch Bharathiar Univ, Dept Biotechnol China Med Univ, Grad Inst Chinese Med Sci |
Keywords: | 17 beta-Estradiol calcineurin cardiac apoptosis isoproterenol apoptosis |
Date: | 2017-04 |
Issue Date: | 2018-11-30 15:52:17 (UTC+8) |
Publisher: | Mdpi Ag |
Abstract: | 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. 17 beta-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/ER beta suppresses apoptosis is not fully understood, and the role of protein phosphatase in E2/ER beta action also needs further investigation. In this study, we observed that E2/ER beta inhibited isoproterenol (ISO)-induced myocardial cell apoptosis, cytochrome c release and downstream apoptotic markers. Moreover, we found that E2/ER beta 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 beta gene may prove to be effective means to treat stress-induced myocardial damage. |
Relation: | International Journal of Molecular Sciences, v.18, n.4, pp.892 |
Appears in Collections: | [Dept. of Hospital and Health (including master's program)] Periodical Articles
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