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Korean Society for Biochemistry and Molecular Biology (생화학분자생물학회)
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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)
  • Received : 2013.08.26
  • Accepted : 2013.11.10
  • Published : 2014.07.31
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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.

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References

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