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Conséquences de l'ischémie/reperfusion sur le pore de transition de perméabilité mitochondrial

Abstract : Several studies have shown that ischemia/reperfusion injury is strongly related to mitochondrial dysfunction. These studies have mostly focused on the involvement of the permeability transition in this phenomenon. The permeability transition is mediated by the opening of the mitochondrial permeability transition pore (mPTP). PTP activation may occur during ischemia or reperfusion. The aim of this work was to visualize mPTP opening during ischemia/reperfusion conditions on intact cells (HMEC-1 and INS-1) and to study its involvement in this phenomenon. For the first time, we observed the opening of the mPTP mediated by ischemia/reperfusion by monitoring the damages caused by its activation (NADH efflux and ΔΨ decrease). This mPTP activation occurred during ischemia in HMEC-1 and INS-1 cells. However, mPTP induction was prevented by cyclosporine A in both cell models. Furthermore, our results showed the involvement of complex I in the prevention of NADH efflux and ΔΨ decrease. A decrease in the mitochondrial calcium retention capacity was also shown in permeabilised cells during ischemia, which disappear after 60 minutes of reperfusion. Thus, the visualisation of the mPTP opening in a model of ischemia / reperfusion is an interesting observation indicating the involvement of PTP in this phenomenon. Furthermore, the study of ischemia in vitro would provide answers regarding the involvement of cellular function changes in tissue damage.
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Zineb Baidi. Conséquences de l'ischémie/reperfusion sur le pore de transition de perméabilité mitochondrial. Sciences agricoles. Université de Grenoble, 2011. Français. ⟨NNT : 2011GRENV059⟩. ⟨tel-00721775⟩

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