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

FEBS Letters

Li, Linjiang¹  Liu, Shu-sen¹  Chen, Quan¹  Wu, Caihong²  Xia, Tian¹  Jiang, Chunsun¹ 

[1] National Key Laboratory of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100080, PR China;National Key Laboratory of Biomembrane and Membrane Biotechnology, Peking University, Beijing 100871, PR China

关键词: Apoptosis;    Mitochondrion;    Caspase-3;    Reactive oxygen species;    Permeability transition pore;    Cytochrome c;    AIF;    apoptosis-inducing factor;    CCCP;    carbonyl cyanide m-chlorophenylhydrazone;    CsA;    cyclosporin A;    cyt c;    cytochrome c;    ΔΨ m;    mitochondrial membrane potential;    PTP;    permeability transition pore;    RCR;    respiratory control ratio;    Rh123;    rhodamine 123;    ROS;    reactive oxygen species;    X;    xanthine;    XO;    xanthine oxidase;   

DOI  :  10.1016/S0014-5793(01)03228-8

学科分类：生物化学/生物物理

来源: John Wiley & Sons Ltd.

【 摘 要 】

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.

【 授权许可】

Unknown