5
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: not found

      The impact of cardiac ischemia/reperfusion on the mitochondria-cytoskeleton interactions.

      Read this article at

      ScienceOpenPublisherPubMed
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          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 (MOM) is an essential element of compartmentalized energy transfer. In adult cardiomyocytes, the MOM permeability to ADP is regulated by the interaction of voltage-dependent anion channel with cytoskeletal proteins, particularly with β 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 β 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, β 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 β 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.

          Related collections

          Author and article information

          Journal
          Biochim. Biophys. Acta
          Biochimica et biophysica acta
          Elsevier BV
          0006-3002
          0006-3002
          June 2016
          : 1862
          : 6
          Affiliations
          [1 ] University Grenoble Alpes, Laboratory of Fundamental and Applied Bioenergetics, INSERM U1055, Grenoble, France; University Grenoble Alpes, TIMC-IMAG, CNRS, UMR5525, Grenoble, France.
          [2 ] University Grenoble Alpes, TIMC-IMAG, CNRS, UMR5525, Grenoble, France.
          [3 ] University Grenoble Alpes, Laboratory of Fundamental and Applied Bioenergetics, INSERM U1055, Grenoble, France.
          [4 ] University Grenoble Alpes, Life Science Imaging - In Vitro Platform, IAB, INSERM CRI U823, Grenoble, France.
          [5 ] INSERM, U836, F-38000, Grenoble, France; University Grenoble Alpes, GIN, F-38000 Grenoble, France.
          [6 ] National Institute of Chemical Physics and Biophysics, Laboratory of Bioenergetics, Tallinn, Estonia.
          [7 ] Innsbruck Medical University, Cardiac Surgery Research Laboratory, Innsbruck A-6020, Austria.
          [8 ] University Grenoble Alpes, Laboratory of Fundamental and Applied Bioenergetics, INSERM U1055, Grenoble, France; Hospital of the University Grenoble Alpes, Department Thorax (EFCR), France. Electronic address: rita.guzun@gmail.com.
          Article
          S0925-4439(16)30055-2
          10.1016/j.bbadis.2016.03.009
          26976332

          Respiration, Mitochondria, Ischemia/reperfusion, Heart, Tubulin

          Comments

          Comment on this article