Article

A study on permeability transition pore opening and cytochrome c release from mitochondria, induced by caspase-3 in vitro.

National Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, P R China.
FEBS Letters (impact factor: 3.54). 02/2002; 510(1-2):62-6. pp.62-6
Source: PubMed

ABSTRACT We recently described that there is a feedback amplification of cytochrome c release from mitochondria by caspases. Here we investigated how caspases impact on mitochondria to induce cytochrome c release and found that recombinant caspase-3 induced opening of permeability transition pore and reduction of membrane potential in vitro. These events were inhibited by Bcl-xL, cyclosporin A and z-VAD.fmk. Moreover, caspase-3 stimulated the rate of mitochondrial state 4 respiration, superoxide production and NAD(P)H oxidation in a Bcl-xL- and cyclosporin A-inhibitable manner. These results suggest that caspase-3 induces cytochrome c release by inducing permeability transition pore opening which is associated with changes in mitochondrial respiration and redox potential.

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Keywords

Bcl-xL
 
Bcl-xL-
 
caspase-3
 
caspase-3 induces cytochrome c release
 
caspases
 
caspases impact
 
cyclosporin
 
cyclosporin A-inhibitable manner
 
cytochrome c release
 
events
 
feedback amplification
 
induce cytochrome c release
 
inducing permeability transition pore opening
 
membrane potential
 
mitochondria
 
mitochondrial respiration
 
mitochondrial state 4 respiration
 
permeability transition pore
 
recombinant caspase-3 induced opening
 
superoxide production