Bagur 2016 Biochim Biophys Acta

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Bagur R, Tanguy S, Foriel S, Grichine A, Sanchez C, Pernet-Gallay K, Kaambre T, Kuznetsov AV, Usson Y, Boucher F, Guzun R (2016) The impact of cardiac ischemia/reperfusion on the mitochondria-cytoskeleton interactions. Biochim Biophys Acta 1862:1159-71.

Β» PMID: 26976332

Bagur R, Tanguy S, Foriel S, Grichine A, Sanchez C, Pernet-Gallay K, Kaambre T, Kuznetsov AV, Usson Y, Boucher F, Guzun R (2016) Biochim Biophys Acta

Abstract: Cardiac ischemia-reperfusion (IR) injury compromises mitochondrial oxidative phosphorylation (OxPhos) and compartmentalized intracellular energy transfer via the phosphocreatine/creatine kinase (CK) network. The restriction of ATP/ADP diffusion at the level of the mitochondrial outer membrane (mtOM) is an essential element of compartmentalized energy transfer. In adult cardiomyocytes, the mtOM permeability to ADP is regulated by the interaction of voltage-dependent anion channel with cytoskeletal proteins, particularly with Ξ² tubulin II. The IR-injury alters the expression and the intracellular arrangement of cytoskeletal proteins. The objective of the present study was to investigate the impact of IR on the intracellular arrangement of Ξ² tubulin II and its effect on the regulation of mitochondrial respiration. Perfused rat hearts were subjected to total ischemia (for 20min (I20) and 45min (I45)) or to ischemia followed by 30min of reperfusion (I20R and I45R groups). High-resolution respirometry and fluorescent confocal microscopy were used to study respiration, Ξ² tubulin II and mitochondrial arrangements in cardiac fibers. The results of these experiments evidence a heterogeneous response of mitochondria to IR-induced damage. Moreover, the intracellular rearrangement of Ξ² tubulin II, which in the control group colocalized with mitochondria, was associated with increased apparent affinity of OxPhos for ADP, decreased regulation of respiration by creatine without altering mitochondrial CK activity and the ratio between octameric to dimeric isoenzymes. The results of this study allow us to highlight changes of mitochondrial interactions with cytoskeleton as one of the possible mechanisms underlying cardiac IR injury.

Copyright Β© 2016 Elsevier B.V. All rights reserved. β€’ Keywords: Heart, Ischemia/reperfusion, Mitochondria, Respiration, Tubulin

β€’ O2k-Network Lab: EE Tallinn Kaambre T, EE Tallinn Saks VA

Labels: MiParea: Respiration  Pathology: Cardiovascular  Stress:Ischemia-reperfusion  Organism: Rat  Tissue;cell: Heart  Preparation: Permeabilized tissue  Enzyme: Complex I  Regulation: ADP  Coupling state: LEAK, OXPHOS  Pathway: N, S  HRR: Oxygraph-2k 


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