Inhibitory effects of Bcl-2 on mitochondrial respiration

Title:

Inhibitory effects of Bcl-2 on mitochondrial respiration

Creator:

Marek Vrbacký, Jan Krijt, Zdeněk Drahota, and Zora Mělková

Identifier:

https://cdk.lib.cas.cz/client/handle/uuid:b0d52666-3b86-4448-9b48-459c314e7f7a
uuid:b0d52666-3b86-4448-9b48-459c314e7f7a
issn:0862-8408

Subject:

Fyziologie člověka a srovnávací fyziologie, apoptóza, apoptosis, Bcl-2, ATP, mitochondrial respiration, 14, and 612

Type:

article, články, model:article, and TEXT

Format:

print, bez média, and svazek

Description:

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., M. Vrbacký, J. Krijt, Z. Drahota, Z. Mělková., and Obsahuje bibliografii

Language:

English

Rights:

http://creativecommons.org/licenses/by-nc-sa/4.0/
policy:public

Source:

Physiological research | 2003 Volume:52 | Number:5

Harvested from:

CDK

Metadata only:

false