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- Title
E2/ER β Enhances Calcineurin Protein Degradation and PI3K/Akt/MDM2 Signal Transduction to Inhibit ISO-Induced Myocardial Cell Apoptosis.
- Authors
Kuan-Ho Lin; Wei-Wen Kuo; Shibu, Marthandam Asokan; Day, Cecilia-Hsuan; You-Liang Hsieh; Li-Chin Chung; Chen, Ray-Jade; Su-Ying Wen; Viswanadha, Vijaya Padma; Chih-Yang Huang
- 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.
- Subjects
CELLULAR signal transduction; PROTEOLYSIS; CALCINEURIN; APOPTOSIS; CARDIAC hypertrophy
- Publication
International Journal of Molecular Sciences, 2017, Vol 18, Issue 4, p892
- ISSN
1661-6596
- Publication type
Article
- DOI
10.3390/ijms18040892