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

Autor:	Gouriou, Yves, Alam, Muhammad Rizwan, Harhous, Zeina, Silva, Claire Crola Da, Baetz, Delphine Baetz, Badawi, Sally, Lefai, Etienne, Rieusset, Jennifer, Durand, Annie, Harisseh, Rania, Gharib, Abdallah, Ovize, Michel, Bidaux, Gabriel
Přispěvatelé:	Cardiovasculaire, métabolisme, diabétologie et nutrition (CarMeN), Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National des Sciences Appliquées de Lyon (INSA Lyon), Institut National des Sciences Appliquées (INSA)-Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hospices Civils de Lyon (HCL), Leducq Transatlantic Network of Excellence16 CVD 04, ANR-10-IBHU-0004,OPeRa,Organ ProtEction and ReplAcement(2010), ANR-16-RHUS-0009,MARVELOUS,MARVELOUS(2016), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Institut National des Sciences Appliquées (INSA)-Institut National des Sciences Appliquées (INSA)-Hospices Civils de Lyon (HCL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Quaid-i-Azam University (QAU), Leducq Transatlantic Network of Excellence 16 CVD 04
Rok vydání:	2020
Předmět:	Membrane Potential Mitochondrial Cell Death hypoxia ANT2 [SDV]Life Sciences [q-bio] Adenine Nucleotide Translocator 2 bioenergetics Mitochondrial Membrane Transport Proteins Article Cell Line Mitochondria Rats IF1 ATP Adenosine Triphosphate mitochondrial membrane potential Mitochondrial Membranes mitochondria-associated membranes Animals mitofusin 2 ATP synthase Calcium Myocytes Cardiac metabolism
Zdroj:	Cells Cells, MDPI, 2020, 9 (12), pp.2542. ⟨10.3390/cells9122542⟩ Volume 9 Issue 12
ISSN:	2073-4409
Popis:	Following a prolonged exposure to hypoxia&ndash 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&ndash 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&ndash reoxygenation challenge.
Databáze:	OpenAIRE
Externí odkaz:	https://explore.openaire.eu/search/publication?articleId=pmid_dedup__::5f910f3ff0a801998420cc8b8ca979e4 https://pubmed.ncbi.nlm.nih.gov/33255741 Zobrazit plný text záznamu Plný text ve formátu PDF Plný text ve formátu HTML
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