Metabolomics and In-Silico Analysis Reveal Critical Energy Deregulations in Animal Models of Parkinson’s Disease
Identifieur interne : 000D45 ( Main/Merge ); précédent : 000D44; suivant : 000D46Metabolomics and In-Silico Analysis Reveal Critical Energy Deregulations in Animal Models of Parkinson’s Disease
Auteurs : Pierre O. Poliquin [Canada] ; Jingkui Chen [Canada] ; Mathieu Cloutier [Canada] ; Louis-Éric Trudeau [Canada] ; Mario Jolicoeur [Canada]Source :
- PLoS ONE [ 1932-6203 ] ; 2013.
English descriptors
- KwdEn :
- Animals, Brain (drug effects), Brain (metabolism), Brain (pathology), Carbonyl Cyanide m-Chlorophenyl Hydrazone (toxicity), Computer Simulation, Disease Models, Animal, Energy Metabolism (drug effects), Metabolomics, Mice, Mice, Knockout, Parkinson Disease (metabolism), Parkinson Disease (pathology), Stress, Physiological (drug effects), Ubiquitin-Protein Ligases (deficiency), Ubiquitin-Protein Ligases (genetics).
- MESH :
- chemical , deficiency : Ubiquitin-Protein Ligases.
- chemical , genetics : Ubiquitin-Protein Ligases.
- chemical , toxicity : Carbonyl Cyanide m-Chlorophenyl Hydrazone.
- drug effects : Brain, Energy Metabolism, Stress, Physiological.
- metabolism : Brain, Parkinson Disease.
- pathology : Brain, Parkinson Disease.
- Animals, Computer Simulation, Disease Models, Animal, Metabolomics, Mice, Mice, Knockout.
Abstract
Parkinson’s disease (PD) is a multifactorial disease known to result from a variety of factors. Although age is the principal risk factor, other etiological mechanisms have been identified, including gene mutations and exposure to toxins. Deregulation of energy metabolism, mostly through the loss of complex I efficiency, is involved in disease progression in both the genetic and sporadic forms of the disease. In this study, we investigated energy deregulation in the cerebral tissue of animal models (genetic and toxin induced) of PD using an approach that combines metabolomics and mathematical modelling. In a first step, quantitative measurements of energy-related metabolites in mouse brain slices revealed most affected pathways. A genetic model of PD, the Park2 knockout, was compared to the effect of CCCP, a complex I blocker. Model simulated and experimental results revealed a significant and sustained decrease in ATP after CCCP exposure, but not in the genetic mice model. In support to data analysis, a mathematical model of the relevant metabolic pathways was developed and calibrated onto experimental data. In this work, we show that a short-term stress response in nucleotide scavenging is most probably induced by the toxin exposure. In turn, the robustness of energy-related pathways in the model explains how genetic perturbations, at least in young animals, are not sufficient to induce significant changes at the metabolite level.
Url:
DOI: 10.1371/journal.pone.0069146
PubMed: 23935941
PubMed Central: 3720533
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PMC:3720533Le document en format XML
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Poliquin</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Jingkui" sort="Chen, Jingkui" uniqKey="Chen J" first="Jingkui" last="Chen">Jingkui Chen</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Cloutier, Mathieu" sort="Cloutier, Mathieu" uniqKey="Cloutier M" first="Mathieu" last="Cloutier">Mathieu Cloutier</name><affiliation wicri:level="1"><nlm:aff id="aff2"><addr-line>GERAD and Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>GERAD and Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Trudeau, Louis Eric" sort="Trudeau, Louis Eric" uniqKey="Trudeau L" first="Louis-Éric" last="Trudeau">Louis-Éric Trudeau</name><affiliation wicri:level="1"><nlm:aff id="aff3"><addr-line>Department of Pharmacology, Faculty of Medicine, Université de Montréal, Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Pharmacology, Faculty of Medicine, Université de Montréal, Montréal, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Jolicoeur, Mario" sort="Jolicoeur, Mario" uniqKey="Jolicoeur M" first="Mario" last="Jolicoeur">Mario Jolicoeur</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23935941</idno><idno type="pmc">3720533</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3720533</idno><idno type="RBID">PMC:3720533</idno><idno type="doi">10.1371/journal.pone.0069146</idno><date when="2013">2013</date><idno type="wicri:Area/Pmc/Corpus">000A94</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000A94</idno><idno type="wicri:Area/Pmc/Curation">000A94</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000A94</idno><idno type="wicri:Area/Pmc/Checkpoint">000628</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000628</idno><idno type="wicri:source">PubMed</idno><idno type="wicri:Area/PubMed/Corpus">000888</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000888</idno><idno type="wicri:Area/PubMed/Curation">000888</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">000888</idno><idno type="wicri:Area/PubMed/Checkpoint">000888</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">000888</idno><idno type="wicri:Area/Ncbi/Merge">001534</idno><idno type="wicri:Area/Ncbi/Curation">001534</idno><idno type="wicri:Area/Ncbi/Checkpoint">001534</idno><idno type="wicri:Area/Main/Merge">000D45</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Metabolomics and <italic>In-Silico</italic> Analysis Reveal Critical Energy Deregulations in Animal Models of Parkinson’s Disease</title><author><name sortKey="Poliquin, Pierre O" sort="Poliquin, Pierre O" uniqKey="Poliquin P" first="Pierre O." last="Poliquin">Pierre O. Poliquin</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Chen, Jingkui" sort="Chen, Jingkui" uniqKey="Chen J" first="Jingkui" last="Chen">Jingkui Chen</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Cloutier, Mathieu" sort="Cloutier, Mathieu" uniqKey="Cloutier M" first="Mathieu" last="Cloutier">Mathieu Cloutier</name><affiliation wicri:level="1"><nlm:aff id="aff2"><addr-line>GERAD and Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>GERAD and Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Trudeau, Louis Eric" sort="Trudeau, Louis Eric" uniqKey="Trudeau L" first="Louis-Éric" last="Trudeau">Louis-Éric Trudeau</name><affiliation wicri:level="1"><nlm:aff id="aff3"><addr-line>Department of Pharmacology, Faculty of Medicine, Université de Montréal, Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Pharmacology, Faculty of Medicine, Université de Montréal, Montréal, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author><author><name sortKey="Jolicoeur, Mario" sort="Jolicoeur, Mario" uniqKey="Jolicoeur M" first="Mario" last="Jolicoeur">Mario Jolicoeur</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Brain (drug effects)</term><term>Brain (metabolism)</term><term>Brain (pathology)</term><term>Carbonyl Cyanide m-Chlorophenyl Hydrazone (toxicity)</term><term>Computer Simulation</term><term>Disease Models, Animal</term><term>Energy Metabolism (drug effects)</term><term>Metabolomics</term><term>Mice</term><term>Mice, Knockout</term><term>Parkinson Disease (metabolism)</term><term>Parkinson Disease (pathology)</term><term>Stress, Physiological (drug effects)</term><term>Ubiquitin-Protein Ligases (deficiency)</term><term>Ubiquitin-Protein Ligases (genetics)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Ubiquitin-Protein Ligases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Carbonyl Cyanide m-Chlorophenyl Hydrazone</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Brain</term><term>Energy Metabolism</term><term>Stress, Physiological</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Computer Simulation</term><term>Disease Models, Animal</term><term>Metabolomics</term><term>Mice</term><term>Mice, Knockout</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Parkinson’s disease (PD) is a multifactorial disease known to result from a variety of factors. Although age is the principal risk factor, other etiological mechanisms have been identified, including gene mutations and exposure to toxins. Deregulation of energy metabolism, mostly through the loss of complex I efficiency, is involved in disease progression in both the genetic and sporadic forms of the disease. In this study, we investigated energy deregulation in the cerebral tissue of animal models (genetic and toxin induced) of PD using an approach that combines metabolomics and mathematical modelling. In a first step, quantitative measurements of energy-related metabolites in mouse brain slices revealed most affected pathways. A genetic model of PD, the Park2 knockout, was compared to the effect of CCCP, a complex I blocker. Model simulated and experimental results revealed a significant and sustained decrease in ATP after CCCP exposure, but not in the genetic mice model. In support to data analysis, a mathematical model of the relevant metabolic pathways was developed and calibrated onto experimental data. In this work, we show that a short-term stress response in nucleotide scavenging is most probably induced by the toxin exposure. In turn, the robustness of energy-related pathways in the model explains how genetic perturbations, at least in young animals, are not sufficient to induce significant changes at the metabolite level.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Goedert, M" uniqKey="Goedert M">M Goedert</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Uversky, Vn" uniqKey="Uversky V">VN Uversky</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Rinne, J" uniqKey="Rinne J">J Rinne</name></author><author><name sortKey="Rummukainen, J" uniqKey="Rummukainen J">J Rummukainen</name></author><author><name sortKey="Paljarvi, L" uniqKey="Paljarvi L">L Paljarvi</name></author><author><name sortKey="Rinne, U" uniqKey="Rinne U">U Rinne</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Bergareche, A" uniqKey="Bergareche A">A 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Sneppen</name></author><author><name sortKey="Lizana, L" uniqKey="Lizana L">L Lizana</name></author><author><name sortKey="Jensen, Mh" uniqKey="Jensen M">MH Jensen</name></author><author><name sortKey="Pigolotti, S" uniqKey="Pigolotti S">S Pigolotti</name></author><author><name sortKey="Otzen, D" uniqKey="Otzen D">D Otzen</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Qi, Z" uniqKey="Qi Z">Z Qi</name></author><author><name sortKey="Miller, Gw" uniqKey="Miller G">GW Miller</name></author><author><name sortKey="Voit, Eo" uniqKey="Voit E">EO Voit</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Vali, S" uniqKey="Vali S">S Vali</name></author><author><name sortKey="Mythri, Rb" uniqKey="Mythri R">RB Mythri</name></author><author><name sortKey="Jagatha, B" uniqKey="Jagatha B">B Jagatha</name></author><author><name sortKey="Padiadpu, J" uniqKey="Padiadpu J">J Padiadpu</name></author><author><name sortKey="Ramanujan, Ks" uniqKey="Ramanujan K">KS Ramanujan</name></author></analytic></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct><analytic><author><name sortKey="Cloutier, M" uniqKey="Cloutier M">M Cloutier</name></author><author><name sortKey="Wellstead, P" uniqKey="Wellstead P">P Wellstead</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Owen, Jb" uniqKey="Owen J">JB Owen</name></author><author><name sortKey="Butterfield, Da" uniqKey="Butterfield D">DA Butterfield</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Cloutier, M" uniqKey="Cloutier M">M Cloutier</name></author><author><name sortKey="Middleton, R" uniqKey="Middleton R">R Middleton</name></author><author><name sortKey="Wellstead, P" uniqKey="Wellstead P">P Wellstead</name></author></analytic></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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