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4 results on '"Maya Allouche"'

1. Burden of Poor Health Conditions and Quality of Life in 656 Children with Primary Immunodeficiency

Author

Capucine Picard, Carolina Brito De Azevedo, Benedicte Neven, Vincent Barlogis, Alain Fischer, Isabelle Pellier, Virginie Gandemer, Maya Allouche, Nizar Mahlaoui, Marlène Pasquet, Pascal Auquier, Fanny Fouyssac, Gérard Michel, Nathalie Aladjidi, Caroline Thomas, Stéphane Blanche, Despina Moshous, Eric Jeziorski, Camille Vercasson, Françoise Mazingue, Pédiatrie et oncologie pédiatrique [Hôpital de la Timone - APHM], Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)- Hôpital de la Timone [CHU - APHM] (TIMONE), Centre de Référence Déficits Immunitaires Héréditaires (CEREDIH), Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-CHU Necker - Enfants Malades [AP-HP], Service d'immuno-hématologie pédiatrique [CHU Necker], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP), Centre Référence des Maladies Héréditaires du Métabolisme de l'Enfant et de l'Adulte [CHU Necker] (MaMEA Necker), CHU Necker - Enfants Malades [AP-HP], Hôpital de la Timone [CHU - APHM] (TIMONE), Centre d'études et de recherche sur les services de santé et la qualité de vie (CEReSS), Aix Marseille Université (AMU), Imagine - Institut des maladies génétiques (IMAGINE - U1163), Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Hôpital Jeanne de Flandres, Université de Lille, Droit et Santé-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Université Paris Descartes - Paris 5 (UPD5), Collège de France (CDF), Collège de France (CdF), Université Sorbonne Paris Cité (USPC), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Necker - Enfants Malades [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Chaire Médecine expérimentale (A. Fischer), Collège de France (CdF (institution)), and Collège de France - Chaire Médecine expérimentale (A. Fischer)

Subjects
Male, Pediatrics, medicine.medical_specialty, Adolescent, [SDV]Life Sciences [q-bio], health status, transition to adulthood, Affect (psychology), primary immunodeficiency, Cohort Studies, 03 medical and health sciences, 0302 clinical medicine, Quality of life, Cost of Illness, Surveys and Questionnaires, Health care, Medicine, Vulnerable population, Humans, 030212 general & internal medicine, Registries, Prospective Studies, Prospective cohort study, Child, Preschool, business.industry, Immunologic Deficiency Syndromes, medicine.disease, 3. Good health, Child, Preschool, 030220 oncology & carcinogenesis, Pediatrics, Perinatology and Child Health, Cohort, Primary immunodeficiency, Quality of Life, Female, France, business, Cohort study, Follow-Up Studies
Abstract

International audience; OBJECTIVE: To gain insight into how primary immunodeficiencies (PIDs) affect children's health status and quality of life. STUDY DESIGN: The French Reference Center for PIDs conducted a prospective multicenter cohort that enrolled participants who met all criteria: patients included in the French Reference Center for PIDs registry, children younger than18 years, and living in France. Participants were asked to complete both a health questionnaire and a health-related quality of life (HR-QoL) questionnaire. A severity score was assigned to each health condition: grade 1 (mild) to grade 4 (life-threatening). HR-QoL in children was compared with age- and sex-matched French norms. RESULTS: Among 1047 eligible children, 656 were included in the study, and 117 had undergone hematopoietic stem cell transplantation; 40% experienced at least one grade 4 condition, and 83% experienced at least one grade 3 or 4 condition. Compared with the French norms, children with PID scored significantly lower for most HR-QoL domains. Low HR-QoL scores were associated strongly with burden of poor conditions. CONCLUSIONS: Our results quantify the magnitude of conditions in children with PID and demonstrate that the deleterious health effects borne by patients already are evident in childhood. These results emphasize the need to closely monitor this vulnerable population and establish multidisciplinary healthcare teams from childhood. TRIAL REGISTRATION: ClinicalTrials.gov: NCT02868333 and EudraCT 2012-A0033-35.

Published
2018
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2. Late cardiomyopathy in childhood acute myeloid leukemia survivors: a study from the LEA program

Author

Gérard Michel, Pascal Chastagner, Guy Leverger, Maya Allouche, Yves Bertrand, Marie-Dominique Tabone, Hervé Chambost, Vincent Barlogis, Camille Vercasson, Laure Saumet, André Baruchel, Sandrine Thouvenin-Doulet, Maryline Poiree, Dominique Plantaz, Pascal Auquier, Justyna Kanold, Julie Berbis, Claire Oudin, Service d'hématologie pédiatrique, Université de la Méditerranée - Aix-Marseille 2-Assistance Publique - Hôpitaux de Marseille (APHM)- Hôpital de la Timone [CHU - APHM] (TIMONE), Santé Publique et maladies Chroniques : Qualité de vie Concepts, Usages et Limites, Déterminants (SPMC), Assistance Publique - Hôpitaux de Marseille (APHM)-Aix Marseille Université (AMU), Service d'hématologie, CHU Lyon, Service d'Hématologie Pédiatrique [CHRU Nancy], Centre Hospitalier Régional Universitaire de Nancy (CHRU Nancy), Service Hématologie Infantile, CHU Grenoble, Service de Pédiatrie, Unité d'Oncologie et Hématologie Pédiatrique, Centre Hospitalier Universitaire de Nice (CHU Nice), CHU Clermont-Ferrand-CIC Inserm 501, Service d'hématologie-immunologie-oncologie pédiatrique [CHU Trousseau], Université Pierre et Marie Curie - Paris 6 (UPMC)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), Centre Hospitalier Universitaire de Saint-Etienne (CHU de Saint-Etienne), CHU Montpellier, Department of Clinical Hematology, Montpellier, France, Service d'hématologie et immunologie pédiatrique, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Robert Debré-Université Paris Diderot - Paris 7 (UPD7), Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM), CHU Trousseau [APHP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Centre Hospitalier Universitaire de Saint-Etienne [CHU Saint-Etienne] (CHU ST-E), and HAL AMU, Administrateur

Subjects
CHILDREN, Kaplan-Meier Estimate, THERAPY, 0302 clinical medicine, Risk Factors, Antineoplastic Combined Chemotherapy Protocols, ADOLESCENTS, Cumulative incidence, Survivors, Child, RISK, Acute leukemia, Incidence, Childhood Acute Myeloid Leukemia, Hematology, Leucemie Enfant & Adolescent program, CANCER, 3. Good health, Leukemia, Myeloid, Acute, 030220 oncology & carcinogenesis, Child, Preschool, France, Cardiomyopathies, medicine.drug, medicine.medical_specialty, Anthracycline, Adolescent, [SDV.CAN]Life Sciences [q-bio]/Cancer, late cardiomyopathy, ANTHRACYCLINE CARDIOTOXICITY, 03 medical and health sciences, [SDV.CAN] Life Sciences [q-bio]/Cancer, Multicenter trial, Internal medicine, medicine, MANAGEMENT, Idarubicin, Humans, Online Only Articles, ACUTE LYMPHOBLASTIC-LEUKEMIA, Cardiotoxicity, business.industry, Infant, Newborn, pediatric acute myeloid leukemia, Infant, Surgery, Transplantation, business, 030215 immunology, Follow-Up Studies
Abstract

International audience; Late cardiomyopathy in childhood acute myeloid leukemia survivors: a study from the L.E.A. program Prognosis of pediatric acute myeloid leukemia (AML) has improved significantly over the past two decades with survival rates now approaching 70%. 1 Therapy consists of a limited number of intensive chemotherapy courses mainly based on cytarabine and anthracycline. 2,3 Many pediatric late anthracycline cardiotoxicity studies have concerned heterogeneous diagnostic groups. Moreover, single childhood cancer studies were mainly conducted in acute lym-phoblastic leukemia, whereas the highest doses of anthra-cycline are given in children with AML. 4-6 We report here a prospective multi-centric study of late cardiotoxicity in 185 patients surviving childhood AML. All were treated after 1989 in French clinical trials using intensive chemotherapy alone or chemotherapy and allogeneic hematopoietic stem cell transplantation (HSCT). L.E.A. (Leucémie Enfant & Adolescent) is a French prospective long-term follow-up program involving all childhood acute leukemia survivors treated in the participating centers since 1980. Details of the programm are provided elsewhere. 7 As of 31 December 2011, 282 childhood AML survivors fulfilled the L.E.A. inclusion criteria and 218 (77.3%) of them agreed to participate. Among these 218, 185 were treated according to one of the 6 multicenter trial protocols ongoing in France after January 1989. All 185 had serial echocardiographic examination as part of their L.E.A. program, and all were included in the present study. All provided written informed consent. Cardiotoxicity was defined by either clinical symptoms of congestive heart failure or by an abnormal echocardiographic left ventricular function. Left ventricular function was considered abnormal when the shortening fraction (SF) was less than 28% or when the left ventricular ejection fraction (LVEF) was less than 55% on 2D echocardiography. 8-10 Cardiotoxicity was classified as late when it started or persisted beyond one year after the completion of first-line treatment. 9 Cumulative anthracycline doses used in each trial are described in the Online Supplementary Table S1, as well as the doxorubicin-equivalent doses using conversion factors of 0.83, 4.0 and 5.0 for daunorubicin, mitoxantrone and idarubicin, respectively. 10,11 Assessment of health status, long-term late effects on health-related quality of life (QoL), and statistical analysis are described in the Online Supplementary Appendix. Characteristics of the study cohort are summarized in Table 1. Median age at the time of AML diagnosis and median follow-up duration to last cardiac evaluation were 6.53 and 9.5 years, respectively. Thirty-seven patients had a history of relapse. Median cumulative anthracycline dose was 372 mg/m² (Online Supplementary Figure S1). Ninety-nine patients were treated by chemotherapy alone, whereas the other 86 patients also received HSCT (57 in first remission, 25 in second remission, and 4 in more advanced disease). Thirty children received total body irradiation (TBI), but only 10 among the 57 transplanted in first remission did so. Median number of echographic evaluations was 3 per patient. Subclinical cardiotoxicity (SCC) was observed in 23 of 185 patients (12.4%) at least once during their follow-up program. Median time from AML diagnosis to SCC detection was 4.40 years. In these 23 patients, the median value of the worst SF was 27% and the median value of the worst LVEF was 52. Only 3 of 23 patients had a worse SF value of less than 25% (2 had 20%; 1 had 24%). Six of 23 received anti-congestive therapy and none had cardiac transplantation. Five of those receiving anti-congestive therapy were still being treated at time of last evaluation, and 4 had more than 28% SF and more than 55% LVEF. Seventeen patients never received treatment: 11 had spontaneous improvement with more than 28% SF and more than 55% LVEF at last evaluation. Finally, at last cardiac evaluation, only 8 patients had an abnormal left ventricular function. Cumulative incidence (CI) of cardiotoxicity, estimated by the Kaplan-Meier method was 16% and 27% at 10 and 15 years, respectively (Figure 1A). CI of anti-conges-tive treatment at the same follow-up times was 5% and 7%. The risk of developing cardiotoxicity depended on a previous history of relapse and on the cumulative anthracy-cline dose. At ten years from diagnosis, CI was 35% versus 11% in patients with or without history of relapse (P=0.02) (Figure 1B). Among 148 patients without any history of relapse, 10-year CI of cardiotoxicity was 14% in 97 patients treated with chemotherapy alone versus 8% in 51 patients who underwent HSCT in first remission (NS, Figure 1C). In transplanted children, the risk was not modified by either a grade 2-4 acute or an extensive chronic graft-versus-host disease. The CI of anti-congestive treatment in these 148 patients who never experienced relapse was 3% at ten and

Published
2015
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3. Glycogen synthase kinase 3-mediated voltage-dependent anion channel phosphorylation controls outer mitochondrial membrane permeability during lipid accumulation

Author

Guido Kroemer, Cécile Martel, Céline Henry, Catherine Brenner, Elena Fanelli, Maya Allouche, Joël Chopineau, Giuseppe Calamita, Davide Degli Esposti, Antoinette Lemoine, Céline Boursier, Université Joseph Fourier - Grenoble 1 (UJF), Institut Charles Gerhardt Montpellier - Institut de Chimie Moléculaire et des Matériaux de Montpellier (ICGM ICMMM), Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM)-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Réponses cellulaires au microenvironnement et cancer, Institut National de la Santé et de la Recherche Médicale (INSERM), Università degli studi di Bari Aldo Moro = University of Bari Aldo Moro (UNIBA), Protéines et Nanotechnologies en Sciences Séparatives, Université Paris-Sud - Paris 11 (UP11), Centre Ressources Autisme de Bourgogne (CHU de Dijon) (CRAB), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Université de Nîmes (UNIMES), Centre de Recherche des Cordeliers (CRC (UMR_S 872)), Université Pierre et Marie Curie - Paris 6 (UPMC)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Apoptose, cancer et immunité (U848), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Institut National de la Santé et de la Recherche Médicale (INSERM), Plateforme de métabolomique, Direction de la recherche [Gustave Roussy], Institut Gustave Roussy (IGR)-Institut Gustave Roussy (IGR), Pôle de biologie, Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Université Paris Descartes - Faculté de Médecine (UPD5 Médecine), Université Paris Descartes - Paris 5 (UPD5), Microenvironnement et Physiopathologie de la Differenciation, Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'Excellence en Recherche sur le Médicament et l'Innovation Thérapeutique [Châtenay-Malabry] (LabEx LERMIT), University of Paris Sud, Institut National pour le Cancer (INCa) [2008-1-PL BIO-04-CNRS ON1], LabEx LERMIT, PRES UniverSud Paris, Association pour la Recherche sur le Cancer, ANR [ANR-08PCVI-0008-01], MIUR [PRIN20089SRS2X_003], Fondazione Cassa di Risparmio di Puglia, Chopineau, Joel, Université Joseph Fourier - Grenoble 1 ( UJF ), Institut Charles Gerhardt Montpellier - Institut de Chimie Moléculaire et des Matériaux de Montpellier ( ICGM ICMMM ), Université Montpellier 1 ( UM1 ) -Université Montpellier 2 - Sciences et Techniques ( UM2 ) -Ecole Nationale Supérieure de Chimie de Montpellier ( ENSCM ) -Université de Montpellier ( UM ) -Centre National de la Recherche Scientifique ( CNRS ), Institut National de la Santé et de la Recherche Médicale ( INSERM ), University of Bari Aldo Moro ( UNIBA ), Université Paris-Sud - Paris 11 ( UP11 ), Centre Ressources Autisme de Bourgogne (CHU de Dijon) ( CRAB ), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand ( CHU Dijon ), Université de Nîmes ( UNIMES ), Centre de Recherche des Cordeliers ( CRC (UMR_S 872) ), Université Pierre et Marie Curie - Paris 6 ( UPMC ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Centre National de la Recherche Scientifique ( CNRS ), Apoptose, cancer et immunité ( U848 ), Université Paris-Sud - Paris 11 ( UP11 ) -Institut Gustave Roussy ( IGR ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Institut Gustave Roussy ( IGR ) -Institut Gustave Roussy ( IGR ), Assistance publique - Hôpitaux de Paris (AP-HP)-Hôpital Européen Georges Pompidou [APHP] ( HEGP ), Université Paris Descartes - Faculté de Médecine ( UPD5 Médecine ), Université Paris Descartes - Paris 5 ( UPD5 ), Université Paris-Sud - Paris 11 ( UP11 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), PRES UniverSud ( CNRS UMR 8159 ), Université de Versailles Saint-Quentin-en-Yvelines ( UVSQ ), Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM)-Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)-Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-Institut de Chimie du CNRS (INC), University of Bari Aldo Moro (UNIBA), and Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Gustave Roussy (IGR)-Université Paris-Sud - Paris 11 (UP11)

Subjects
Male, MESH : Fatty Liver, MESH : Hepatocytes, Mitochondrion, ACTIVATION, MESH: Hepatocytes, Glycogen Synthase Kinase 3, Mice, MESH : Phosphorylation, 0302 clinical medicine, MESH: Mitochondrial Membranes, MESH : Lipid Metabolism, GSK-3, Voltage-Dependent Anion Channels, MESH : Female, MESH: Animals, Phosphorylation, MESH: Fatty Liver, Cells, Cultured, MESH: Glycogen Synthase Kinase 3, MESH: Lipid Metabolism, 0303 health sciences, INSULIN-RESISTANCE, biology, VDAC, MESH : Voltage-Dependent Anion Channels, NONALCOHOLIC STEATOHEPATITIS, Fatty liver, 3. Good health, Cell biology, APOPTOSIS, [SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biophysics, Lipotoxicity, Biochemistry, 030220 oncology & carcinogenesis, MESH: Calcium, Mitochondrial Membranes, Female, MESH: Cells, Cultured, [ SDV.BBM.BP ] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biophysics, Voltage-dependent anion channel, MESH : Glycogen Synthase Kinase 3, MESH : Male, bcl-X Protein, INHIBITION, [SDV.BBM.BP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biophysics, MESH : Mice, Inbred C57BL, macromolecular substances, MESH: bcl-X Protein, 03 medical and health sciences, MESH : Mitochondrial Membranes, MESH: Mice, Inbred C57BL, LIVER STEATOSIS, MESH : Mice, MESH : Cells, Cultured, medicine, Animals, Humans, TRANSITION PORE, MODULATION, MESH : Calcium, MESH: Mice, 030304 developmental biology, MESH: Humans, Hepatology, MESH: Phosphorylation, MESH : bcl-X Protein, MESH : Humans, MESH: Voltage-Dependent Anion Channels, Lipid metabolism, Lipid Metabolism, medicine.disease, MESH: Male, Fatty Liver, Mice, Inbred C57BL, CELL-DEATH, Hepatocytes, biology.protein, Calcium, MESH : Animals, Steatosis, MESH: Female
Abstract

International audience; UNLABELLED: Nonalcoholic steatosis is a liver pathology characterized by fat accumulation and severe metabolic alterations involving early mitochondrial impairment and late hepatocyte cell death. However, mitochondrial dysfunction mechanisms remain elusive. Using four models of nonalcoholic steatosis, i.e., livers from patients with fatty liver disease, ob/ob mice, mice fed a high-fat diet, and in vitro models of lipotoxicity, we show that outer mitochondrial membrane permeability is altered and identified a posttranslational modification of voltage-dependent anion channel (VDAC), a membrane channel and NADH oxidase, as a cause of early mitochondrial dysfunction. Thus, in nonalcoholic steatosis VDAC exhibits reduced threonine phosphorylation, which increases the influx of water and calcium into mitochondria, sensitizes the organelle to matrix swelling, depolarization, and cytochrome c release without inducing cell death. This also amplifies VDAC enzymatic and channel activities regulation by calcium and modifies its interaction with proteic partners. Moreover, lipid accumulation triggers a rapid lack of VDAC phosphorylation by glycogen synthase kinase 3 (GSK3). Pharmacological and genetic manipulations proved GSK3 to be responsible for VDAC phosphorylation in normal cells. Notably, VDAC phosphorylation level correlated with steatosis severity in patients. CONCLUSION: VDAC acts as an early sensor of lipid toxicity and its GSK3-mediated phosphorylation status controls outer mitochondrial membrane permeabilization in hepatosteatosis.

Published
2013
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4. ANT-VDAC1 interaction is direct and depends on ANT isoform conformation in vitro

Author

Céline Henry, Maya Allouche, Cécile Martel, Ossama Sharaf el dein, Nathalie Saint, Catherine Brenner, Joël Chopineau, Jean-Luc Robert, Claire Pertuiset, Remi Veneziano, Institut Charles Gerhardt Montpellier - Institut de Chimie Moléculaire et des Matériaux de Montpellier (ICGM ICMMM), Ecole Nationale Supérieure de Chimie de Montpellier (ENSCM)-Centre National de la Recherche Scientifique (CNRS)-Université de Montpellier (UM)-Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-Institut de Chimie du CNRS (INC), Université de Nîmes (UNIMES), Université Joseph Fourier - Grenoble 1 (UJF), Centre Ressources Autisme de Bourgogne (CHU de Dijon) (CRAB), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Physiologie & médecine expérimentale du Cœur et des Muscles [U 1046] (PhyMedExp), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), l'Agence Nationale pour la Recherche [ANR-08PCVI-0008-01], and ANR [ANR-10-LABX-33]

Subjects
MEMBRANE-PROTEIN VDAC, Protein Conformation, Mitochondrion, MESH: Voltage-Dependent Anion Channel 1, Biochemistry, MESH: Recombinant Proteins, 0302 clinical medicine, Protein structure, MESH: Protein Conformation, CHANNEL, MESH: Animals, reproductive and urinary physiology, 0303 health sciences, biology, Adenine nucleotide translocator, food and beverages, ADENINE-NUCLEOTIDE TRANSLOCATOR, MUSCLE, Recombinant Proteins, ANT, Mitochondria, Cell biology, MESH: Surface Plasmon Resonance, Isoenzymes, Liposome, [SDV.BBM.BP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biophysics, TARGET, behavior and behavior mechanisms, MESH: Isoenzymes, PERMEABILITY TRANSITION PORE, MESH: Mitochondrial ADP, ATP Translocases, MESH: Immobilized Proteins, VDAC1, Gene isoform, CARBOXYATRACTYLOSIDE, EXPRESSION, Voltage-dependent anion channel, MESH: Rats, MESH: Mitochondria, Biophysics, 03 medical and health sciences, Surface plasmon resonance, Animals, Humans, Immunoprecipitation, Inner membrane, MITOCHONDRIAL ADP/ATP CARRIER, Molecular Biology, 030304 developmental biology, COMPLEX, MESH: Humans, MESH: Immunoprecipitation, Voltage-Dependent Anion Channel 1, fungi, Cell Biology, biochemical phenomena, metabolism, and nutrition, Rats, Immobilized Proteins, biology.protein, Mitochondrial ADP, ATP Translocases, 030217 neurology & neurosurgery
Abstract

International audience; The voltage-dependent anion channel (VDAC) and the adenine nucleotide translocase (ANT) have central roles in mitochondrial functions such as nucleotides transport and cell death. The interaction between VDAC, an outer mitochondrial membrane protein and ANT, an inner membrane protein, was studied in isolated mitochondria and in vitro. Both proteins were isolated from various mitochondrial sources and reconstituted in vitro using a biomimetic system composed of recombinant human VDAC isoform 1 (rhVDAC1) immobilized on a surface plasmon resonance (SPR) sensor chip surface. Two enriched-preparations of (H)ANT (ANT from heart, mainly ANT1) and (L)ANT (ANT from liver, mainly ANT2) isoforms interacted differently with rhVDAC1. Moreover, the pharmacological ANT inhibitors atractyloside and bongkrekic acid modulated this interaction. Thus, ANT-VDAC interaction depends both on ANT isoform identity and on the conformation of ANT.

Published
2012
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