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Mechanism of mitochondrial respiratory control in caspase-3 induced positive feedback loop in apoptosis
Authors:Tian?Xia  Chunsun?Jiang  Linjiang?Li  Quan?Chen  Email author" target="_blank">Caihong?WuEmail author  Email author" target="_blank">Shusen?LiuEmail author
Institution:(1) National Key Lab of Biomembrane and Membrane Biotechnology, Peking University, 100871 Beijing, China;(2) National Key Lab of Biomembrane and Membrane Biotechnology, Institute of Zoology, Chinese Academy of Sciences, 100080 Beijing, China;(3) Tianjin Sports Institute, 300381 Tianjin, China
Abstract:Caspase-3 plays a central role in the execution of apoptosis. Besides many substrates of caspase-3, mitochondria seem to be one of the candidate targets in the apoptotic process. We evaluated the effects of caspase-3 on the isolated mitochondria in detail, and especially focused on the mechanism involved in mitochondrial functions, which were not fully assessed till now. Our results showed that recombinant caspase-3 induced the increase of superoxide production, the dissipation of mitochondrial membrane potential and rate increasing of mitochondrial state 4 respiration. Caspases inhibitor, z-VAD-fmk can inhibit these effects of caspase-3 on mitochondria. Bcl-xL and cyclosporin A were also shown to be able to inhibit these changes. These results suggested a possible mechanism in caspase-3 induced disruption of mitochondrial membrane barrier which formed a positive feedback loop in apoptosis.
Keywords:mitochondria  caspase-3  ROS  RCR  membrane potential  PTP
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