NDLI: Akt mediates 17β-estradiol and/or estrogen receptor-α inhibition of LPS-induced tumor necresis factor-α expression and myocardial cell apoptosis by suppressing the JNK1/2-NFκB pathway

Content Provider	PubMed Central
Author	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 Huang, Chih-yang
Copyright Year	2009
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.
Related Links	http://dx.doi.org/10.1111/j.1582-4934.2009.00669.x
Ending Page	3667
Page Count	13
Starting Page	3655
File Format	PDF
ISSN	15821838
e-ISSN	15824934
Journal	Journal of Cellular and Molecular Medicine
Issue Number	9b
Volume Number	13
Language	English
Publisher	John Wiley & Sons, Ltd
Publisher Date	2009-09-01
Access Restriction	Open
Rights Holder	John Wiley & Sons, Ltd
Subject Keyword	Molecular Medicine Cell Biology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Molecular Medicine

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