PMID- 26976332
OWN - NLM
STAT- MEDLINE
DCOM- 20190508
LR  - 20190508
IS  - 0006-3002 (Print)
IS  - 0006-3002 (Linking)
VI  - 1862
IP  - 6
DP  - 2016 Jun
TI  - The impact of cardiac ischemia/reperfusion on the mitochondria-cytoskeleton 
      interactions.
PG  - 1159-71
LID - S0925-4439(16)30055-2 [pii]
LID - 10.1016/j.bbadis.2016.03.009 [doi]
AB  - 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 beta 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 beta 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, beta 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 beta 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.
CI  - Copyright (c) 2016 Elsevier B.V. All rights reserved.
FAU - Bagur, Rafaela
AU  - Bagur R
AD  - University Grenoble Alpes, Laboratory of Fundamental and Applied Bioenergetics, 
      INSERM U1055, Grenoble, France; University Grenoble Alpes, TIMC-IMAG, CNRS, 
      UMR5525, Grenoble, France.
FAU - Tanguy, Stephane
AU  - Tanguy S
AD  - University Grenoble Alpes, TIMC-IMAG, CNRS, UMR5525, Grenoble, France.
FAU - Foriel, Sarah
AU  - Foriel S
AD  - University Grenoble Alpes, Laboratory of Fundamental and Applied Bioenergetics, 
      INSERM U1055, Grenoble, France.
FAU - Grichine, Alexei
AU  - Grichine A
AD  - University Grenoble Alpes, Life Science Imaging - In Vitro Platform, IAB, INSERM 
      CRI U823, Grenoble, France.
FAU - Sanchez, Caroline
AU  - Sanchez C
AD  - University Grenoble Alpes, TIMC-IMAG, CNRS, UMR5525, Grenoble, France.
FAU - Pernet-Gallay, Karin
AU  - Pernet-Gallay K
AD  - INSERM, U836, F-38000, Grenoble, France; University Grenoble Alpes, GIN, F-38000 
      Grenoble, France.
FAU - Kaambre, Tuuli
AU  - Kaambre T
AD  - National Institute of Chemical Physics and Biophysics, Laboratory of 
      Bioenergetics, Tallinn, Estonia.
FAU - Kuznetsov, Andrey V
AU  - Kuznetsov AV
AD  - Innsbruck Medical University, Cardiac Surgery Research Laboratory, Innsbruck 
      A-6020, Austria.
FAU - Usson, Yves
AU  - Usson Y
AD  - University Grenoble Alpes, TIMC-IMAG, CNRS, UMR5525, Grenoble, France.
FAU - Boucher, Francois
AU  - Boucher F
AD  - University Grenoble Alpes, TIMC-IMAG, CNRS, UMR5525, Grenoble, France.
FAU - Guzun, Rita
AU  - Guzun R
AD  - 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.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20160311
PL  - Netherlands
TA  - Biochim Biophys Acta
JT  - Biochimica et biophysica acta
JID - 0217513
RN  - 0 (Tubulin)
SB  - IM
MH  - Animals
MH  - Cell Respiration
MH  - Cytoskeleton/metabolism/*pathology
MH  - Heart Ventricles/metabolism/pathology/physiopathology
MH  - Male
MH  - Mitochondria, Heart/metabolism/*pathology
MH  - Myocardial Reperfusion Injury/metabolism/*pathology/physiopathology
MH  - Myocardium/metabolism/*pathology
MH  - Rats, Wistar
MH  - Tubulin/*metabolism/ultrastructure
OTO - NOTNLM
OT  - Heart
OT  - Ischemia/reperfusion
OT  - Mitochondria
OT  - Respiration
OT  - Tubulin
EDAT- 2016/03/16 06:00
MHDA- 2019/05/09 06:00
CRDT- 2016/03/16 06:00
PHST- 2015/06/13 00:00 [received]
PHST- 2016/02/18 00:00 [revised]
PHST- 2016/03/10 00:00 [accepted]
PHST- 2016/03/16 06:00 [entrez]
PHST- 2016/03/16 06:00 [pubmed]
PHST- 2019/05/09 06:00 [medline]
AID - S0925-4439(16)30055-2 [pii]
AID - 10.1016/j.bbadis.2016.03.009 [doi]
PST - ppublish
SO  - Biochim Biophys Acta. 2016 Jun;1862(6):1159-71. doi: 
      10.1016/j.bbadis.2016.03.009. Epub 2016 Mar 11.