Document Detail


Inhibitory effects of Bcl-2 on mitochondrial respiration.
MedLine Citation:
PMID:  14535829     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In contrast to the well-established anti-apoptotic effect of Bcl-2 protein, we have recently demonstrated that Bcl-2 overexpression by vaccinia virus causes apoptosis in BSC-40 cells, while it prevents apoptosis in HeLa G cells. Given the key role of mitochondria in the process of apoptosis, we focused on effects of Bcl-2 expression on mitochondrial energetics of these two cell lines. In this study we present data indicating that BSC-40 cells derive their ATP mainly from oxidative phosphorylation whereas HeLa G cells from glycolysis. More importantly, we show that in both cell lines, Bcl-2 inhibits mitochondrial respiration and causes a decrease of the ATP/ADP ratio. However, it appears that BSC-40 cells cannot sustain this decrease and die, while HeLa G cells survive, being adapted to the low ratio of ATP/ADP maintained by glycolysis. Based on this observation, we propose that the outcome of Bcl-2 expression is determined by the type of cellular ATP synthesis, namely that Bcl-2 causes apoptosis in cells relying on oxidative phosphorylation.
Authors:
M Vrbacký; J Krijt; Z Drahota; Z Mĕlková
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Physiological research / Academia Scientiarum Bohemoslovaca     Volume:  52     ISSN:  0862-8408     ISO Abbreviation:  Physiol Res     Publication Date:  2003  
Date Detail:
Created Date:  2003-10-10     Completed Date:  2004-07-14     Revised Date:  2008-04-02    
Medline Journal Info:
Nlm Unique ID:  9112413     Medline TA:  Physiol Res     Country:  Czech Republic    
Other Details:
Languages:  eng     Pagination:  545-54     Citation Subset:  IM    
Affiliation:
Department of Immunology and Microbiology, First Faculty of Medicine of Charles University, Studnickova 7, 128 00 Prague 2, Czech Republic.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Diphosphate / metabolism
Adenosine Triphosphate / metabolism
Animals
Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone / pharmacology
Cell Line, Transformed
Cell Respiration / drug effects,  physiology*
Digitonin / pharmacology
Gene Expression
Hela Cells
Humans
Mitochondria / drug effects,  physiology*
Oligomycins / pharmacology
Oxygen Consumption / drug effects
Proto-Oncogene Proteins c-bcl-2 / genetics,  physiology*
Rotenone / pharmacology
Succinic Acid / pharmacology
Transfection
Chemical
Reg. No./Substance:
0/Oligomycins; 0/Proto-Oncogene Proteins c-bcl-2; 110-15-6/Succinic Acid; 11024-24-1/Digitonin; 370-86-5/Carbonyl Cyanide p-Trifluoromethoxyphenylhydrazone; 56-65-5/Adenosine Triphosphate; 58-64-0/Adenosine Diphosphate; 83-79-4/Rotenone

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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