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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/8373


    Title: Akt mediates 17 beta-estradiol and/or estrogen receptor-alpha inhibition of LPS-induced tumor necresis factor-alpha expression and myocardial cell apoptosis by suppressing the JNK1/2-NF kappa B pathway
    Authors: Liu, CJ (Liu, Chung-Jung);Lo, JF (Lo, Jeng-Fan);Kuo, CH (Kuo, Chia-Hua);Chu, CH (Chu, Chun-Hsien);Chen, LM (Chen, Li-Ming);Tsai, FJ (Tsai, Fuu-Jen);Tsai, CH (Tsai, Chang-Hai);Tzang, BS (Tzang, Bor-Show);Kuo, WW (Kuo, Wei-Wen);Huang, CY (Huang, Chih-Yang)
    Contributors: 保健系
    Keywords: myocardial cell apoptosis;17 beta-estradiol;estrogen receptor-alpha;PI3K;Akt;NF kappa B;I kappa B;JNK;lipopolysacchride
    Date: 2009-09
    Issue Date: 2010-03-26 10:46:11 (UTC+8)
    Publisher: Asia University
    Abstract: Evidence shows that women have lower tumour necrosis factor-alpha (TNF-alpha) levels and lower incidences of heart dysfunction and sepsis-related morbidity and mortality. To identify the cardioprotective effects and precise cellular/molecular mechanisms behind estrogen and estrogen receptors (ERs), we investigated the effects of 17 beta-estradiol (E-2) and estrogen receptor alpha (ER alpha) on LPS-induced apoptosis by analyzing the activation of survival and death signalling pathways in doxycycline (Dox)-inducible Tet-On/ER alpha H9c2 myocardial cells and ER alpha-transfected primary cardiomyocytes overexpressing ER alpha. We found that LPS challenge activated JNK1/2, and then induced I kappa B degradation, NF kappa B activation, TNF-alpha up-regulation and subsequent myocardial apoptotic responses. In addition, treatments involving E-2, membrane-impermeable BSA-E-2 and/or Dox, which induces ER alpha overexpression, significantly inhibited LPS-induced apoptosis by suppressing LPS-up-regulated JNK1/2 activity, I kappa B degradation, NF kappa B activation and pro-apoptotic proteins (e.g. TNF-alpha, active caspases-8, t-Bid, Bax, released cytochrome c, active caspase-9, active caspase-3) in myocardial cells. However, the cardioprotective properties of E-2, BSA-E-2 and ER alpha overexpression to inhibit LPS-induced apoptosis and promote cell survival were attenuated by applying LY294002 (PI3K inhibitor) and PI3K siRNA. These findings suggest that E-2, BSA-E-2 and ER alpha expression exert their cardioprotective effects by inhibiting JNK1/2-mediated LPS-induced TNF-alpha expression and cardiomyocyte apoptosis through activation of Akt.
    Relation: JOURNAL OF CELLULAR AND MOLECULAR MEDICINE 13 (9B): 3655-3667
    Appears in Collections:[食品營養與保健生技學系] 期刊論文

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