Difference between revisions of "Pasdois 2006 J Bioenerg Biomembr"
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{{Publication | {{Publication | ||
|title=Pasdois P, Beauvoit B, Tariosse L, Vinassa B, Bonoron-Adèle 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- | |title=Pasdois P, Beauvoit B, Tariosse L, Vinassa B, Bonoron-Adèle 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. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/17031549 PMID: 17031549] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/17031549 PMID: 17031549] | ||
|authors=Pasdois P, Beauvoit B, Tariosse L, Vinassa B, Bonoron-Adele S, Santos PD | |authors=Pasdois P, Beauvoit B, Tariosse L, Vinassa B, Bonoron-Adele S, Santos PD | ||
|year=2006 | |year=2006 | ||
|journal=J | |journal=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. | |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, Diazoxide, Ischemic preconditioning, Succinate dehydrogenase, Complex II | |keywords=MitokATP, Diazoxide, Ischemic preconditioning, Succinate dehydrogenase, Complex II | ||
|mipnetlab= | |mipnetlab=FR Pessac Diolez P | ||
|discipline=Biomedicine | |discipline=Biomedicine | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Rat | |||
|tissues=Heart | |||
|preparations=Permeabilized tissue | |||
|injuries=Ischemia-reperfusion | |||
|couplingstates=OXPHOS | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Biomedicine | |discipline=Biomedicine | ||
}} | }} | ||
Latest revision as of 12:42, 16 February 2018
| Pasdois P, Beauvoit B, Tariosse L, Vinassa B, Bonoron-Adèle 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. • Keywords: MitokATP, Diazoxide, Ischemic preconditioning, Succinate dehydrogenase, Complex II
• O2k-Network Lab: FR Pessac Diolez P
Labels:
Stress:Ischemia-reperfusion Organism: Rat Tissue;cell: Heart Preparation: Permeabilized tissue
Coupling state: OXPHOS
HRR: Oxygraph-2k
