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

doi:10.3390/ijms18040892

CNU IR > College of Smart Living > Dept. of Hospital and Health (including master's program) > Periodical Articles > Item 310902800/31670

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

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

Files in This Item:

File	Description	Size	Format
ijms18040892.pdf		2393Kb	Adobe PDF	0	View/Open
index.html		0Kb	HTML	1468	View/Open

Loading...