Difference between revisions of "Pasdois 2006 J Bioenerg Biomembr"
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|abstract=It has been proposed that activation of the mitochondrial ATP-sensitive potassium channel (mitoKATP) is part of signaling pathways triggering the cardioprotection afforded by ischemic preconditioning of the heart. This work was to analyze the mitochondrial function profile of Langendorff-perfused rat hearts during the different phases of various ischemia-reperfusion protocols. Specifically, skinned fibers of ischemic preconditioned hearts exhibit a decline in the succinate-supported respiration and complex II activity during ischemia, followed by a recovery during reperfusion. Meanwhile, the apparent affinity of respiration for ADP (which reflects the matrix volume expansion) is increased during preconditioning stimulus and, to a larger extent, during prolonged ischemia. This evolution pattern is mimicked by diazoxide and abolished by 5-hydroxydecanoate. It is concluded that opening the mitoKATP channel mediates the preservation of mitochondrial structure-function via a mitochondrial matrix shrinkage and a reversible inactivation of complex II during prolonged ischemic insult. | |abstract=It has been proposed that activation of the mitochondrial ATP-sensitive potassium channel (mitoKATP) is part of signaling pathways triggering the cardioprotection afforded by ischemic preconditioning of the heart. This work was to analyze the mitochondrial function profile of Langendorff-perfused rat hearts during the different phases of various ischemia-reperfusion protocols. Specifically, skinned fibers of ischemic preconditioned hearts exhibit a decline in the succinate-supported respiration and complex II activity during ischemia, followed by a recovery during reperfusion. Meanwhile, the apparent affinity of respiration for ADP (which reflects the matrix volume expansion) is increased during preconditioning stimulus and, to a larger extent, during prolonged ischemia. This evolution pattern is mimicked by diazoxide and abolished by 5-hydroxydecanoate. It is concluded that opening the mitoKATP channel mediates the preservation of mitochondrial structure-function via a mitochondrial matrix shrinkage and a reversible inactivation of complex II during prolonged ischemic insult. | ||
|keywords=MitokATP,ย Diazoxide, Ischemic preconditioning, Succinate dehydrogenase, Complex II | |keywords=MitokATP,ย Diazoxide, Ischemic preconditioning, Succinate dehydrogenase, Complex II | ||
|mipnetlab= | |mipnetlab=FR Pessac Beauvoit B | ||
|discipline=Biomedicine | |discipline=Biomedicine | ||
}} | }} |
Revision as of 14:53, 24 March 2015
Pasdois P, Beauvoit B, Tariosse L, Vinassa B, Bonoron-Adรจle S, Santos PD (2006) MitoK(ATP)-dependent changes in mitochondrial volume and in complex II activity during ischemic and pharmacological preconditioning of Langendorff-perfused rat heart. J Bioenerg Biomembr 38:101-12. |
Pasdois P, Beauvoit B, Tariosse L, Vinassa B, Bonoron-Adele S, Santos PD (2006) J Bioenerg Biomembr
Abstract: It has been proposed that activation of the mitochondrial ATP-sensitive potassium channel (mitoKATP) is part of signaling pathways triggering the cardioprotection afforded by ischemic preconditioning of the heart. This work was to analyze the mitochondrial function profile of Langendorff-perfused rat hearts during the different phases of various ischemia-reperfusion protocols. Specifically, skinned fibers of ischemic preconditioned hearts exhibit a decline in the succinate-supported respiration and complex II activity during ischemia, followed by a recovery during reperfusion. Meanwhile, the apparent affinity of respiration for ADP (which reflects the matrix volume expansion) is increased during preconditioning stimulus and, to a larger extent, during prolonged ischemia. This evolution pattern is mimicked by diazoxide and abolished by 5-hydroxydecanoate. It is concluded that opening the mitoKATP channel mediates the preservation of mitochondrial structure-function via a mitochondrial matrix shrinkage and a reversible inactivation of complex II during prolonged ischemic insult. โข Keywords: MitokATP, Diazoxide, Ischemic preconditioning, Succinate dehydrogenase, Complex II
โข O2k-Network Lab: FR Pessac Beauvoit B
Labels:
Stress:Ischemia-reperfusion;preservation"Ischemia-reperfusion;preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Rat Tissue;cell: Heart Preparation: Permeabilized tissue
Coupling state: OXPHOS
HRR: Oxygraph-2k