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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/31670


    標題: E2/ER beta Enhances Calcineurin Protein Degradation and PI3K/Akt/MDM2 Signal Transduction to Inhibit ISO-Induced Myocardial Cell Apoptosis
    作者: 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
    貢獻者: 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
    關鍵字: 17 beta-Estradiol
    calcineurin
    cardiac apoptosis
    isoproterenol
    apoptosis
    日期: 2017-04
    上傳時間: 2018-11-30 15:52:17 (UTC+8)
    出版者: Mdpi Ag
    摘要: 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.
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