Vrbacky 2003 Physiol Res: Difference between revisions
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{{Publication | {{Publication | ||
|title= | |title=Vrbackรฝ M, Krijt J, Drahota Z, Mฤlkovรก Z (2003) Inhibitory effects of Bcl-2 on mitochondrial respiration. Physiol Res 52:545-54. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/14535829 PMID: 14535829] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/14535829 PMID: 14535829 Open Access] | ||
|authors=Vrbacky M, Krijt J, Drahota Z, Melkova Z | |authors=Vrbacky M, Krijt J, Drahota Z, Melkova Z | ||
|year=2003 | |year=2003 | ||
Line 7: | Line 7: | ||
|abstract=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. | |abstract=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. | ||
|keywords=Bcl-2, Apoptosis, ATP, Mitochondrial respiration | |keywords=Bcl-2, Apoptosis, ATP, Mitochondrial respiration | ||
|mipnetlab=CZ Prague Houstek J, CZ | |mipnetlab=CZ Prague Houstek J, CZ Hradec Kralove Cervinkova Z | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration, Genetic knockout;overexpression, mt-Medicine | |||
|injuries=Cell death | |||
|organism=Human, Other mammals | |||
|tissues=Endothelial;epithelial;mesothelial cell, Other cell lines, HeLa | |||
|preparations=Permeabilized cells, Intact cells | |||
|topics=ATP, Substrate | |||
|couplingstates=ROUTINE, OXPHOS, ET | |||
|pathways=N, S | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
| | |additional=Virus, | ||
}} | }} |
Latest revision as of 15:02, 23 February 2020
Vrbackรฝ M, Krijt J, Drahota Z, Mฤlkovรก Z (2003) Inhibitory effects of Bcl-2 on mitochondrial respiration. Physiol Res 52:545-54. |
Vrbacky M, Krijt J, Drahota Z, Melkova Z (2003) Physiol Res
Abstract: 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. โข Keywords: Bcl-2, Apoptosis, ATP, Mitochondrial respiration
โข O2k-Network Lab: CZ Prague Houstek J, CZ Hradec Kralove Cervinkova Z
Labels: MiParea: Respiration, Genetic knockout;overexpression, mt-Medicine
Stress:Cell death Organism: Human, Other mammals Tissue;cell: Endothelial;epithelial;mesothelial cell, Other cell lines, HeLa Preparation: Permeabilized cells, Intact cells
Regulation: ATP, Substrate Coupling state: ROUTINE, OXPHOS, ET Pathway: N, S HRR: Oxygraph-2k
Virus