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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16304

    Title: Akt Mediates 17β-Estradiol and/or Estrogen Receptor Inhibition of LPS-Induced Tumor Necrosis Factor-αExpression and Myocardial Cell Apoptosis by Suppressing the JNK1/2 and NFkB Pathway
    Authors: ;Liu, Chung-Jung;Lo, Jeng-Fan;Kuo, Chia-Hua;Chu, Chun-Hsien;Chen, Li-Ming;Tsai, Fuu-Jen;Tsai, Chang-Hai;Tzang, Bor-Show;Kuo, Wei-Wen;黃志揚;HUANG, CHIH-YANG
    Contributors: 生物科技學系
    Date: 2009-02
    Issue Date: 2012-11-23 17:11:13 (UTC+8)
    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 17beta-estradiol (E(2)) and estrogen receptor alpha (ERalpha) on LPS-induced apoptosis by analyzing the activation of survival and death signalling pathways in doxycycline (Dox)-inducible Tet-On/ERalpha H9c2 myocardial cells and ERalpha-transfected primary cardiomyocytes overexpressing ERalpha. We found that LPS challenge activated JNK1/2, and then induced IkappaB degradation, NFkappaB 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 ERalpha overexpression, significantly inhibited LPS-induced apoptosis by suppressing LPS-up-regulated JNK1/2 activity, IkappaB degradation, NFkappaB 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 ERalpha 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 ERalpha expression exert their cardioprotective effects by inhibiting JNK1/2-mediated LPS-induced TNF-alpha expression and cardiomyocyte apoptosis through activation of Akt.
    Appears in Collections:[生物科技學系] 期刊論文

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