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http://dx.doi.org/10.5483/BMBRep.2014.47.7.194

BI-1 enhances Fas-induced cell death through a Na+/H+-associated mechanism  

Lee, Geum-Hwa (Department of Pharmacology, School of Medicine, Chonbuk National University)
Kim, Hyung-Ryong (Department of Dental Pharmacology, Wonkwang Dental Research Institute, School of Dentistry, Wonkwang University)
Chae, Han-Jung (Department of Pharmacology, School of Medicine, Chonbuk National University)
Publication Information
BMB Reports / v.47, no.7, 2014 , pp. 393-398 More about this Journal
Abstract
The role of Bax inhibitor-1 (BI-1) in the protective mechanism against apoptotic stimuli has been studied; however, as little is known about its role in death receptor-mediated cell death, this study was designed to investigate the effect of BI-1 on Fas-induced cell death, and the underlying mechanisms. HT1080 adenocarcinoma cells were cultured in high concentration of glucose media and transfected with vector alone (Neo cells) or BI-1-vector (BI-1 cells), and treated with Fas. In cell viability, apoptosis, and caspase-3 analyses, the BI-1 cells showed enhanced sensitivity to Fas. Fas significantly decreased cytosolic pH in BI-1 cells, compared with Neo cells, and this decrease correlated with BI-1 oligomerization, mitochondrial $Ca^{2+}$ accumulation, and significant inhibition of sodium-hydrogen exchanger (NHE) activity. Compared with Neo cells, a single treatment of BI-1 cells with the NHE inhibitor EIPA or siRNA against NHE significantly increased cell death, which suggests that the viability of BI-1 cells is affected by the maintenance of intracellular pH homeostasis through NHE.
Keywords
Bax inhibitor-1; Cancer; Cell death; Fas; Sodium-hydrogen exchanger;
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