English  |  正體中文  |  简体中文  |  Items with full text/Total items : 90453/105672 (86%)
Visitors : 13195681      Online Users : 503
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/310904400/111541

    Title: Estrogen and/or Estrogen Receptor Inhibits BNIP3-Induced Apoptosis and Autophagy in H9c2 Cardiomyoblast Cells
    Authors: 陳必誠;Chen, Bih-Cheng;Weng, Yi-Jiun;Weng, Yi-Jiun;徐布;Shibu, Marthandam Asokan;韓建國;Han, Chien-Kuo;Yueh-Sheng, C;Chen, Yueh-Sheng;She, Chia-Yao;Shen, Chia-Yao;Lin, Yueh-Min;Lin, Yueh-Min;Padma, Vijaya;Viswanadha, Vijaya Padma;Li, Hsin-Yueh;Liang, Hsin-Yueh;黃志揚;Huang, Chih-yang;*
    Contributors: 生物科技學系
    Keywords: BNIP3, estrogen receptor alpha, apoptosis, autophagy
    Date: 2018-04
    Issue Date: 2018-10-22 11:25:28 (UTC+8)
    Abstract: The process of autophagy in heart cells maintains homeostasis during cellular stress such as hypoxia by removing aggregated proteins and damaged organelles and thereby protects the heart during the times of starvation and ischemia. However, autophagy can lead to substantial cell death under certain circumstances. BCL2/adenovirus E1B 19 kDa protein-interacting protein 3 (BNIP3), a hypoxia-induced marker, has been shown to induce both autophagy and apoptosis. A BNIP3-docked organelle, e.g., mitochondria, also determines whether autophagy or apoptosis will take place. Estrogen (E2) and estrogen receptor (ER) alpha (ERα) have been shown to protect the heart against mitochondria-dependent apoptosis. The aim of the present study is to investigate the mechanisms by which ERα regulates BNIP3-induced apoptosis and autophagy, which is associated with hypoxic injury, in cardiomyoblast cells. An in vitro model to mimic hypoxic injury in the heart by engineering H9c2 cardiomyoblast cells to overexpress BNIP3 was established. Further, the effects of E2 and ERα in BNIP3-induced apoptosis and autophagy were determined in BNIP3 expressing H9c2 cells. Results from TUNEL assay and Immunoflourecense assay for LC3 puncta formation, respectively, revealed that ERα/E2 suppresses BNIP3-induced apoptosis and autophagy. The Western blot analysis showed ERα/E2 decreases the protein levels of caspase 3 (apoptotic marker), Atg5, and LC3-II (autophagic markers). Co-immunoprecipitation of BNIP3 and immunoblotting of Bcl-2 and Rheb showed that ERα reduced the interaction between BNIP3 and Bcl-2 or Rheb. The results confirm that ERα binds to BNIP3 causing a reduction in the levels of functional BNIP3 and thereby inhibits cellular apoptosis and autophagy. In addition, ERα attenuated the activity of the BNIP3 promoter by binding to SP-1 or NFκB sites.
    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