English  |  正體中文  |  简体中文  |  Items with full text/Total items : 92472/107804 (86%)
Visitors : 19143723      Online Users : 669
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version

    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/111547

    Title: 17β-Estradiol and/or estrogen receptor alpha signaling blocks protein phosphatase 1 mediated ISO induced cardiac hypertrophy
    Authors: Fa, Hsin-Yuan;Fang, Hsin-Yuan;Hung, Meng-Yu;Hung, Meng-Yu;Hung, Meng-Yu;Hung, Meng-Yu;Pande, Sudhir;Pandey, Sudhir;Chia-Chien, Chia-Chien C;Chang, Chia-Chien;Lin, Kuan-Ho;Lin, Kuan-Ho;She, Chia-Yao;Shen, Chia-Yao;Padma, Vijaya;Viswanadha, Vijaya Padma;Kuo, Wei-Wen;Kuo, Wei-Wen;黃志揚;Huang, Chih-Yang;*
    Contributors: 生物科技學系
    Date: 2018-05
    Issue Date: 2018-10-22 11:25:59 (UTC+8)
    Abstract: Earlier studies have shown that estrogen possess protective function against the development of pathological cardiac hypertrophy. However, the molecular mechanisms of estrogens (E2) protective effect are poorly understood. Additionally, abnormal activation of β-adrenergic signaling have been implicated in the development of pathological cardiac remodeling. However, the role of serine/threonine protein phosphatase 1 (PP1) in pathological cardiac remodeling under the influence of β-adrenergic signaling have been sparsely investigated. In this study, we assessed the downstream effects of abnormal activation of PP1 upon isoproterenol (ISO) induced pathological cardiac changes. We found that pre-treatment of 17β-estradiol (E2), tet-on estrogen receptor-α, or both significantly inhibited ISO-induced increase in cell size, hypertrophy marker gene expression and cytosolic calcium accumulation in H9c2 cells. Additionally, treatment with estrogen receptor inhibitor (ICI) reversed those effects, implicating role of E2 in inhibiting pathological cardiac remodeling. However, specific inhibition of ERα using melatonin, reduced ISO-induced PP1c expression and enhanced the level of ser-16 phosphorylated phospholamban (PLB), responsible for regulation of sarcoplasmic reticulum Ca2+-ATPase (SERCA) activity. Furthermore, hypertrophic effect caused by overexpression of PP1cα was reduced by treatment with specific inhibitor of ERα. Collectively, we found that estrogen and estrogen receptor-α have protective effect against pathological cardiac changes by suppressing PP1 expression and its downstream signaling pathway, which further needs to be elucidated.
    Relation: PLoS One
    Appears in Collections:[生物科技學系] 期刊論文

    Files in This Item:

    File SizeFormat

    All items in ASIAIR are protected by copyright, with all rights reserved.

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback