Metabolomics and in-silico analysis reveal critical energy deregulations in animal models of Parkinson's disease.
Identifieur interne : 000888 ( PubMed/Corpus ); précédent : 000887; suivant : 000889Metabolomics and in-silico analysis reveal critical energy deregulations in animal models of Parkinson's disease.
Auteurs : Pierre O. Poliquin ; Jingkui Chen ; Mathieu Cloutier ; Louis-Éric Trudeau ; Mario JolicoeurSource :
- 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 mitochondrial uncoupler [corrected]. 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.
DOI: 10.1371/journal.pone.0069146
PubMed: 23935941
Links to Exploration step
pubmed:23935941Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Metabolomics and in-silico 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><nlm:affiliation>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Jingkui" sort="Chen, Jingkui" uniqKey="Chen J" first="Jingkui" last="Chen">Jingkui Chen</name></author><author><name sortKey="Cloutier, Mathieu" sort="Cloutier, Mathieu" uniqKey="Cloutier M" first="Mathieu" last="Cloutier">Mathieu Cloutier</name></author><author><name sortKey="Trudeau, Louis Eric" sort="Trudeau, Louis Eric" uniqKey="Trudeau L" first="Louis-Éric" last="Trudeau">Louis-Éric Trudeau</name></author><author><name sortKey="Jolicoeur, Mario" sort="Jolicoeur, Mario" uniqKey="Jolicoeur M" first="Mario" last="Jolicoeur">Mario Jolicoeur</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2013">2013</date><idno type="RBID">pubmed:23935941</idno><idno type="pmid">23935941</idno><idno type="doi">10.1371/journal.pone.0069146</idno><idno type="wicri:Area/PubMed/Corpus">000888</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000888</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Metabolomics and in-silico 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><nlm:affiliation>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Chen, Jingkui" sort="Chen, Jingkui" uniqKey="Chen J" first="Jingkui" last="Chen">Jingkui Chen</name></author><author><name sortKey="Cloutier, Mathieu" sort="Cloutier, Mathieu" uniqKey="Cloutier M" first="Mathieu" last="Cloutier">Mathieu Cloutier</name></author><author><name sortKey="Trudeau, Louis Eric" sort="Trudeau, Louis Eric" uniqKey="Trudeau L" first="Louis-Éric" last="Trudeau">Louis-Éric Trudeau</name></author><author><name sortKey="Jolicoeur, Mario" sort="Jolicoeur, Mario" uniqKey="Jolicoeur M" first="Mario" last="Jolicoeur">Mario Jolicoeur</name></author></analytic><series><title level="j">PloS one</title><idno type="eISSN">1932-6203</idno><imprint><date when="2013" type="published">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">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 mitochondrial uncoupler [corrected]. 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.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">23935941</PMID><DateCreated><Year>2013</Year><Month>08</Month><Day>12</Day></DateCreated><DateCompleted><Year>2014</Year><Month>03</Month><Day>05</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Electronic-Print"><Journal><ISSN IssnType="Electronic">1932-6203</ISSN><JournalIssue CitedMedium="Internet"><Volume>8</Volume><Issue>7</Issue><PubDate><Year>2013</Year></PubDate></JournalIssue><Title>PloS one</Title><ISOAbbreviation>PLoS ONE</ISOAbbreviation></Journal><ArticleTitle>Metabolomics and in-silico analysis reveal critical energy deregulations in animal models of Parkinson's disease.</ArticleTitle><Pagination><MedlinePgn>e69146</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.pone.0069146</ELocationID><Abstract><AbstractText>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 mitochondrial uncoupler [corrected]. 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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Poliquin</LastName><ForeName>Pierre O</ForeName><Initials>PO</Initials><AffiliationInfo><Affiliation>Department of Chemical Engineering, École Polytechnique de Montréal, Montréal, Quebec, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chen</LastName><ForeName>Jingkui</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Cloutier</LastName><ForeName>Mathieu</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Trudeau</LastName><ForeName>Louis-Éric</ForeName><Initials>LÉ</Initials></Author><Author ValidYN="Y"><LastName>Jolicoeur</LastName><ForeName>Mario</ForeName><Initials>M</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><Agency>Canadian Institutes of Health Research</Agency><Country>Canada</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2013</Year><Month>07</Month><Day>23</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS One</MedlineTA><NlmUniqueID>101285081</NlmUniqueID><ISSNLinking>1932-6203</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>555-60-2</RegistryNumber><NameOfSubstance UI="D002258">Carbonyl Cyanide m-Chlorophenyl Hydrazone</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="D044767">Ubiquitin-Protein Ligases</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.2.27</RegistryNumber><NameOfSubstance UI="C111567">parkin 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