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    ASIA unversity > 醫學暨健康學院 > 期刊論文 >  Item 310904400/6757

    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/6757

    Title: Akt Mediates 17beta-Estradiol and/or Estrogen Receptor alpha Inhibition of LPS-Induced Tumor Necrosis Factor-alpha Expression and Myocardial Cell Apoptosis by Suppressing the JNK1/2-NFkappaB Pathway
    Authors: Chung-Jung Liu;Jeng-Fan Lo;Chia-Hua Kuo;Chun-Hsien Chu;Li-Ming Chen;Fuu-Jen Tsai;Chang-Hai Tsai;Bor-Show Tzang;Wei-Wen Kuo;Chih-Yang Huang
    Date: 2009
    Issue Date: 2009-12-23 14:22:05 (UTC+8)
    Publisher: Asia University
    Abstract: Evidence shows that women have lower tumour necrosis factor-α (TNF-α) 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 17β-estradiol (E2) and estrogen receptor α (ERα) on LPS-induced apoptosis by analyzing the activation of survival and death signalling pathways in doxycycline (Dox)-inducible Tet-On/ERα H9c2 myocardial cells and ERα-transfected primary cardiomyocytes overexpressing ERα. We found that LPS challenge activated JNK1/2, and then induced IκB degradation, NFκB activation, TNF-α up-regulation and subsequent myocardial apoptotic responses. In addition, treatments involving E2, membrane-impermeable BSA-E2 and/or Dox, which induces ERα overexpression, significantly inhibited LPS-induced apoptosis by suppressing LPS-up-regulated JNK1/2 activity, IκB degradation, NFκB activation and pro-apoptotic proteins (e.g. TNF-α, active caspases-8, t-Bid, Bax, released cytochrome c, active caspase-9, active caspase-3) in myocardial cells. However, the cardioprotective properties of E2, BSA-E2 and ERα overexpression to inhibit LPS-induced apoptosis and promote cell survival were attenuated by applying LY294002 (PI3K inhibitor) and PI3K siRNA. These findings suggest that E2, BSA-E2 and ERα expression exert their cardioprotective effects by inhibiting JNK1/2-mediated LPS-induced TNF-α expression and cardiomyocyte apoptosis through activation of Akt.
    Appears in Collections:[醫學暨健康學院] 期刊論文

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