Vrbacky 2003 Physiol Res

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VrbackΓ½ M, Krijt J, Drahota Z, MΔ•lkovΓ‘ Z (2003) Inhibitory effects of Bcl-2 on mitochondrial respiration. Physiol Res 52:545-54.

Β» PMID: 14535829 Open Access

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. β€’ Keywords: Bcl-2, Apoptosis, ATP, Mitochondrial respiration

β€’ 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 


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