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

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ID: 268628
2017
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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. 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.
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Authors Kuan-Ho Lin;Wei-Wen Kuo;Marthandam Asokan Shibu;Cecilia-Hsuan Day;You-Liang Hsieh;Li-Chin Chung;Ray-Jade Chen;Su-Ying Wen;Vijaya Padma Viswanadha;Chih-Yang Huang;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;
Journal International journal of molecular sciences
Year 2017
DOI
10.3390/ijms18040892
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