Document Detail


Down-modulation of Bis sensitizes cell death in C6 glioma cells induced by oxygen-glucose deprivation.
MedLine Citation:
PMID:  20599823     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Bcl-2 interacting cell death suppressor (Bis), also known as Bag3, has been implicated in anti-stress and anti-apoptotic pathways. In a previous study, we observed a significant induction of Bis in reactive astrocytes of the rat hippocampus after transient forebrain ischemia. To investigate the significance of this induction in ischemic injury, the expression of Bis was reduced with siRNA in C6 glioma cells and exposed to oxygen-glucose deprivation (OGD) conditions. Bis knock-down resulted in an increase in the cell death rate of the C6 cells after OGD, accompanied by accumulation of reactive oxygen species. Among the cellular antioxidants, the induction of superoxide dismutase (SOD) activity was significantly interfered within the cells treated with bis siRNA treated cells (bis-kd C6). A Western blot assay revealed that SOD1 expression gradually increased in control cells, which was not observed in bis-kd cells upon OGD treatment. A quantitative analysis of Sod1 and Sod2 transcripts indicated that the induction of Sod1 was more evidently suppressed by the reduction of Bis. As a transcription factor candidate for the Sod1 gene, the activity of NF-kappaB was determined the nuclear translocation of p65, showing that the activation of NF-kappaB was attenuated in bis-kd C6. Supporting this, an overexpression of Bis augments the activation of NF-kappaB and Sod1 mRNA with an increased cell survival under OGD conditions. These results suggest that one of physiological significances of Bis induction in reactive astrocytes after ischemia in vivo is to protect glial cells from oxidative stress, probably via the induction of SOD1, which is related to the activation of NF-kappaB.
Authors:
Seung Eun Jung; Yong Kwan Kim; Dong-Ye Youn; Mi-Hyun Lim; Jeong Heon Ko; Young Soo Ahn; Jeong-Hwa Lee
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-07-01
Journal Detail:
Title:  Brain research     Volume:  1349     ISSN:  1872-6240     ISO Abbreviation:  Brain Res.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-08-03     Completed Date:  2010-11-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1-10     Citation Subset:  IM    
Copyright Information:
Copyright 2010 Elsevier B.V. All rights reserved.
Affiliation:
Department of Biochemistry, College of Medicine, The Catholic University of Korea, Seoul, Korea.
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MeSH Terms
Descriptor/Qualifier:
Acetylcysteine / pharmacology
Adaptor Proteins, Signal Transducing / genetics,  metabolism*
Animals
Anoxia*
Apoptosis Regulatory Proteins / genetics,  metabolism*
Catalase / metabolism
Cell Death / drug effects
Cell Line, Tumor
Down-Regulation / drug effects,  physiology*
Electrophoretic Mobility Shift Assay / methods
Free Radical Scavengers / pharmacology
Glioma / pathology
Glucose / deficiency*
L-Lactate Dehydrogenase / metabolism
NF-kappa B / metabolism
RNA, Messenger / metabolism
RNA, Small Interfering / pharmacology
Rats
Reactive Oxygen Species / metabolism
Superoxide Dismutase / genetics,  metabolism
Chemical
Reg. No./Substance:
0/Adaptor Proteins, Signal Transducing; 0/Apoptosis Regulatory Proteins; 0/BAG3 protein, rat; 0/Free Radical Scavengers; 0/NF-kappa B; 0/RNA, Messenger; 0/RNA, Small Interfering; 0/Reactive Oxygen Species; 50-99-7/Glucose; 616-91-1/Acetylcysteine; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 1.11.1.6/Catalase; EC 1.15.1.1/Superoxide Dismutase

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