• Laura Cellier, Sophie Tamareille, Hussein Kalakech, Sophie Guillou, Guy Lenaers, Fabrice Prunier, and Delphine Mirebeau-Prunier.
• *L'UNAM Université, Université d'Angers, EA 3860 Cardioprotection Remodelage et Thrombose †L'UNAM Université, Université d'Angers, INSERM U1083, CNRS UMR 6214 ‡CHU Angers, Service de Cardiologie §CHU Angers, Département de Biochimie et Génétique, Angers, France.
• Shock. 2016 Feb 1; 45 (2): 192-7.

AbstractRemote ischemic preconditioning (RIPC) has emerged as an attractive strategy to protect the heart against ischemia-reperfusion (I/R) injury. The mechanisms by which remote ischemic conditioning (RIC) is protective are to date unknown, yet a well-accepted theory holds that the mitochondria play a central role. Mitochondria are dynamic organelles that undergo fusion and fission. Interventions that decrease mitochondrial fission or increase mitochondrial fusion have been associated with reduced I/R injury. However, whether RIPC influences mitochondrial dynamics or not has yet to be ascertained.We sought to determine the role played by mitochondrial dynamics in RIPC-induced cardioprotection. Male adult rats exposed in vivo to myocardial I/R were assigned to one of two groups, either undergoing 40 min of myocardial ischemia followed by 120 min of reperfusion (MI group) or four 5-min cycles of limb ischemia interspersed by 5 min of limb reperfusion, immediately prior to myocardial ischemia and 120 min of reperfusion (MI+RIPC group). After reperfusion, infarct size was assessed and myocardial tissue was analyzed by Western blot and electron microscopy. RIPC induced smaller infarct size (-28%), increased mitochondrial fusion protein OPA1, and preserved mitochondrial morphology. These findings suggest that mitochondrial dynamics play a role in the mechanisms of RIPC-induced cardioprotection.

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