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ANT2-Mediated ATP Import into Mitochondria Protects against Hypoxia Lethal Injury

1
Univ-Lyon, CarMeN Laboratory, INSERM 1060, INRA 1397, Université Claude Bernard Lyon1, INSA Lyon, Oullins, France, IHU OPERA, Groupement Hospitalier EST, Bâtiment B13, 59 boulevard Pinel, F-69500 Bron, France
2
Department of Biochemistry, Quaid-i-Azam University, Islamabad 45320, Pakistan
3
Gilbert and Rose-Marie Chagoury, School of Medicine, Lebanese American University, Byblos 4M8F+8X, Lebanon
*
Authors to whom correspondence should be addressed.
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Cells 2020, 9(12), 2542; https://doi.org/10.3390/cells9122542
Received: 2 October 2020 / Revised: 12 November 2020 / Accepted: 24 November 2020 / Published: 25 November 2020
(This article belongs to the Section Cell Signaling and Regulated Cell Death)
Following a prolonged exposure to hypoxia–reoxygenation, a partial disruption of the ER-mitochondria tethering by mitofusin 2 (MFN2) knock-down decreases the Ca2+ transfer between the two organelles limits mitochondrial Ca2+ overload and prevents the Ca2+-dependent opening of the mitochondrial permeability transition pore, i.e., limits cardiomyocyte cell death. The impact of the metabolic changes resulting from the alteration of this Ca2+crosstalk on the tolerance to hypoxia–reoxygenation injury remains partial and fragmented between different field of expertise. >In this study, we report that MFN2 loss of function results in a metabolic switch driven by major modifications in energy production by mitochondria. During hypoxia, mitochondria maintain their ATP concentration and, concomitantly, the inner membrane potential by importing cytosolic ATP into mitochondria through an overexpressed ANT2 protein and by decreasing the expression and activity of the ATP hydrolase via IF1. This adaptation further blunts the detrimental hyperpolarisation of the inner mitochondrial membrane (IMM) upon re-oxygenation. These metabolic changes play an important role to attenuate cell death during a prolonged hypoxia–reoxygenation challenge. View Full-Text
Keywords: mitofusin 2; mitochondria-associated membranes; hypoxia; metabolism; bioenergetics; ATP; ANT2; ATP synthase; IF1; mitochondrial membrane potential mitofusin 2; mitochondria-associated membranes; hypoxia; metabolism; bioenergetics; ATP; ANT2; ATP synthase; IF1; mitochondrial membrane potential
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MDPI and ACS Style

Gouriou, Y.; Alam, M.R.; Harhous, Z.; Crola Da Silva, C.; Baetz, D.B.; Badawi, S.; Lefai, E.; Rieusset, J.; Durand, A.; Harisseh, R.; Gharib, A.; Ovize, M.; Bidaux, G. ANT2-Mediated ATP Import into Mitochondria Protects against Hypoxia Lethal Injury. Cells 2020, 9, 2542. https://doi.org/10.3390/cells9122542

AMA Style

Gouriou Y, Alam MR, Harhous Z, Crola Da Silva C, Baetz DB, Badawi S, Lefai E, Rieusset J, Durand A, Harisseh R, Gharib A, Ovize M, Bidaux G. ANT2-Mediated ATP Import into Mitochondria Protects against Hypoxia Lethal Injury. Cells. 2020; 9(12):2542. https://doi.org/10.3390/cells9122542

Chicago/Turabian Style

Gouriou, Yves; Alam, Muhammad R.; Harhous, Zeina; Crola Da Silva, Claire; Baetz, Delphine B.; Badawi, Sally; Lefai, Etienne; Rieusset, Jennifer; Durand, Annie; Harisseh, Rania; Gharib, Abdallah; Ovize, Michel; Bidaux, Gabriel. 2020. "ANT2-Mediated ATP Import into Mitochondria Protects against Hypoxia Lethal Injury" Cells 9, no. 12: 2542. https://doi.org/10.3390/cells9122542

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