DJ-1 protects the nigrostriatal axis from the neurotoxin MPTP by modulation of the AKT pathway.
Identifieur interne : 000D75 ( PubMed/Corpus ); précédent : 000D74; suivant : 000D76DJ-1 protects the nigrostriatal axis from the neurotoxin MPTP by modulation of the AKT pathway.
Auteurs : Hossein Aleyasin ; Maxime W C. Rousseaux ; Paul C. Marcogliese ; Sarah J. Hewitt ; Isabella Irrcher ; Alvin P. Joselin ; Mohammad Parsanejad ; Raymond H. Kim ; Patrizia Rizzu ; Steve M. Callaghan ; Ruth S. Slack ; Tak W. Mak ; David S. ParkSource :
- Proceedings of the National Academy of Sciences of the United States of America [ 1091-6490 ] ; 2010.
English descriptors
- KwdEn :
- 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (metabolism), Analysis of Variance, Animals, Blotting, Western, Cell Fractionation, Cells, Cultured, Hydrogen Peroxide (metabolism), Immunohistochemistry, Mice, Neurons (metabolism), Neurotoxins (metabolism), Oncogene Proteins (metabolism), Oxidative Stress (physiology), Peroxiredoxins, Phosphorylation, Protein Deglycase DJ-1, Proto-Oncogene Proteins c-akt (metabolism), Signal Transduction (physiology).
- MESH :
- chemical , metabolism : 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Hydrogen Peroxide, Neurotoxins, Oncogene Proteins, Proto-Oncogene Proteins c-akt.
- metabolism : Neurons.
- physiology : Oxidative Stress, Signal Transduction.
- Analysis of Variance, Animals, Blotting, Western, Cell Fractionation, Cells, Cultured, Immunohistochemistry, Mice, Peroxiredoxins, Phosphorylation, Protein Deglycase DJ-1.
Abstract
Loss-of-function DJ-1 (PARK7) mutations have been linked with a familial form of early onset Parkinson disease. Numerous studies have supported the role of DJ-1 in neuronal survival and function. Our initial studies using DJ-1-deficient neurons indicated that DJ-1 specifically protects the neurons against the damage induced by oxidative injury in multiple neuronal types and degenerative experimental paradigms, both in vitro and in vivo. However, the manner by which oxidative stress-induced death is ameliorated by DJ-1 is not completely clear. We now present data that show the involvement of DJ-1 in modulation of AKT, a major neuronal prosurvival pathway induced upon oxidative stress. We provide evidence that DJ-1 promotes AKT phosphorylation in response to oxidative stress induced by H(2)O(2) in vitro and in vivo following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment. Moreover, we show that DJ-1 is necessary for normal AKT-mediated protective effects, which can be bypassed by expression of a constitutively active form of AKT. Taken together, these data suggest that DJ-1 is crucial for full activation of AKT upon oxidative injury, which serves as one explanation for the protective effects of DJ-1.
DOI: 10.1073/pnas.0914876107
PubMed: 20133695
Links to Exploration step
pubmed:20133695Le document en format XML
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Park</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2010">2010</date><idno type="RBID">pubmed:20133695</idno><idno type="pmid">20133695</idno><idno type="doi">10.1073/pnas.0914876107</idno><idno type="wicri:Area/PubMed/Corpus">000D75</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000D75</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">DJ-1 protects the nigrostriatal axis from the neurotoxin MPTP by modulation of the AKT pathway.</title><author><name sortKey="Aleyasin, Hossein" sort="Aleyasin, Hossein" uniqKey="Aleyasin H" first="Hossein" last="Aleyasin">Hossein Aleyasin</name><affiliation><nlm:affiliation>Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.</nlm:affiliation></affiliation></author><author><name sortKey="Rousseaux, Maxime W C" sort="Rousseaux, Maxime W C" uniqKey="Rousseaux M" first="Maxime W C" last="Rousseaux">Maxime W C. Rousseaux</name></author><author><name sortKey="Marcogliese, Paul C" sort="Marcogliese, Paul C" uniqKey="Marcogliese P" first="Paul C" last="Marcogliese">Paul C. Marcogliese</name></author><author><name sortKey="Hewitt, Sarah J" sort="Hewitt, Sarah J" uniqKey="Hewitt S" first="Sarah J" last="Hewitt">Sarah J. Hewitt</name></author><author><name sortKey="Irrcher, Isabella" sort="Irrcher, Isabella" uniqKey="Irrcher I" first="Isabella" last="Irrcher">Isabella Irrcher</name></author><author><name sortKey="Joselin, Alvin P" sort="Joselin, Alvin P" uniqKey="Joselin A" first="Alvin P" last="Joselin">Alvin P. Joselin</name></author><author><name sortKey="Parsanejad, Mohammad" sort="Parsanejad, Mohammad" uniqKey="Parsanejad M" first="Mohammad" last="Parsanejad">Mohammad Parsanejad</name></author><author><name sortKey="Kim, Raymond H" sort="Kim, Raymond H" uniqKey="Kim R" first="Raymond H" last="Kim">Raymond H. Kim</name></author><author><name sortKey="Rizzu, Patrizia" sort="Rizzu, Patrizia" uniqKey="Rizzu P" first="Patrizia" last="Rizzu">Patrizia Rizzu</name></author><author><name sortKey="Callaghan, Steve M" sort="Callaghan, Steve M" uniqKey="Callaghan S" first="Steve M" last="Callaghan">Steve M. Callaghan</name></author><author><name sortKey="Slack, Ruth S" sort="Slack, Ruth S" uniqKey="Slack R" first="Ruth S" last="Slack">Ruth S. Slack</name></author><author><name sortKey="Mak, Tak W" sort="Mak, Tak W" uniqKey="Mak T" first="Tak W" last="Mak">Tak W. Mak</name></author><author><name sortKey="Park, David S" sort="Park, David S" uniqKey="Park D" first="David S" last="Park">David S. Park</name></author></analytic><series><title level="j">Proceedings of the National Academy of Sciences of the United States of America</title><idno type="eISSN">1091-6490</idno><imprint><date when="2010" type="published">2010</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (metabolism)</term><term>Analysis of Variance</term><term>Animals</term><term>Blotting, Western</term><term>Cell Fractionation</term><term>Cells, Cultured</term><term>Hydrogen Peroxide (metabolism)</term><term>Immunohistochemistry</term><term>Mice</term><term>Neurons (metabolism)</term><term>Neurotoxins (metabolism)</term><term>Oncogene Proteins (metabolism)</term><term>Oxidative Stress (physiology)</term><term>Peroxiredoxins</term><term>Phosphorylation</term><term>Protein Deglycase DJ-1</term><term>Proto-Oncogene Proteins c-akt (metabolism)</term><term>Signal Transduction (physiology)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</term><term>Hydrogen Peroxide</term><term>Neurotoxins</term><term>Oncogene Proteins</term><term>Proto-Oncogene Proteins c-akt</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Neurons</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Oxidative Stress</term><term>Signal Transduction</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Animals</term><term>Blotting, Western</term><term>Cell Fractionation</term><term>Cells, Cultured</term><term>Immunohistochemistry</term><term>Mice</term><term>Peroxiredoxins</term><term>Phosphorylation</term><term>Protein Deglycase DJ-1</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Loss-of-function DJ-1 (PARK7) mutations have been linked with a familial form of early onset Parkinson disease. Numerous studies have supported the role of DJ-1 in neuronal survival and function. Our initial studies using DJ-1-deficient neurons indicated that DJ-1 specifically protects the neurons against the damage induced by oxidative injury in multiple neuronal types and degenerative experimental paradigms, both in vitro and in vivo. However, the manner by which oxidative stress-induced death is ameliorated by DJ-1 is not completely clear. We now present data that show the involvement of DJ-1 in modulation of AKT, a major neuronal prosurvival pathway induced upon oxidative stress. We provide evidence that DJ-1 promotes AKT phosphorylation in response to oxidative stress induced by H(2)O(2) in vitro and in vivo following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment. Moreover, we show that DJ-1 is necessary for normal AKT-mediated protective effects, which can be bypassed by expression of a constitutively active form of AKT. Taken together, these data suggest that DJ-1 is crucial for full activation of AKT upon oxidative injury, which serves as one explanation for the protective effects of DJ-1.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">20133695</PMID><DateCreated><Year>2010</Year><Month>02</Month><Day>17</Day></DateCreated><DateCompleted><Year>2010</Year><Month>05</Month><Day>10</Day></DateCompleted><DateRevised><Year>2017</Year><Month>02</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1091-6490</ISSN><JournalIssue CitedMedium="Internet"><Volume>107</Volume><Issue>7</Issue><PubDate><Year>2010</Year><Month>Feb</Month><Day>16</Day></PubDate></JournalIssue><Title>Proceedings of the National Academy of Sciences of the United States of America</Title><ISOAbbreviation>Proc. Natl. Acad. Sci. U.S.A.</ISOAbbreviation></Journal><ArticleTitle>DJ-1 protects the nigrostriatal axis from the neurotoxin MPTP by modulation of the AKT pathway.</ArticleTitle><Pagination><MedlinePgn>3186-91</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1073/pnas.0914876107</ELocationID><Abstract><AbstractText>Loss-of-function DJ-1 (PARK7) mutations have been linked with a familial form of early onset Parkinson disease. Numerous studies have supported the role of DJ-1 in neuronal survival and function. Our initial studies using DJ-1-deficient neurons indicated that DJ-1 specifically protects the neurons against the damage induced by oxidative injury in multiple neuronal types and degenerative experimental paradigms, both in vitro and in vivo. However, the manner by which oxidative stress-induced death is ameliorated by DJ-1 is not completely clear. We now present data that show the involvement of DJ-1 in modulation of AKT, a major neuronal prosurvival pathway induced upon oxidative stress. We provide evidence that DJ-1 promotes AKT phosphorylation in response to oxidative stress induced by H(2)O(2) in vitro and in vivo following 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment. Moreover, we show that DJ-1 is necessary for normal AKT-mediated protective effects, which can be bypassed by expression of a constitutively active form of AKT. Taken together, these data suggest that DJ-1 is crucial for full activation of AKT upon oxidative injury, which serves as one explanation for the protective effects of DJ-1.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Aleyasin</LastName><ForeName>Hossein</ForeName><Initials>H</Initials><AffiliationInfo><Affiliation>Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, ON K1H 8M5, Canada.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Rousseaux</LastName><ForeName>Maxime W C</ForeName><Initials>MW</Initials></Author><Author ValidYN="Y"><LastName>Marcogliese</LastName><ForeName>Paul C</ForeName><Initials>PC</Initials></Author><Author ValidYN="Y"><LastName>Hewitt</LastName><ForeName>Sarah J</ForeName><Initials>SJ</Initials></Author><Author ValidYN="Y"><LastName>Irrcher</LastName><ForeName>Isabella</ForeName><Initials>I</Initials></Author><Author ValidYN="Y"><LastName>Joselin</LastName><ForeName>Alvin P</ForeName><Initials>AP</Initials></Author><Author ValidYN="Y"><LastName>Parsanejad</LastName><ForeName>Mohammad</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>Kim</LastName><ForeName>Raymond H</ForeName><Initials>RH</Initials></Author><Author ValidYN="Y"><LastName>Rizzu</LastName><ForeName>Patrizia</ForeName><Initials>P</Initials></Author><Author ValidYN="Y"><LastName>Callaghan</LastName><ForeName>Steve M</ForeName><Initials>SM</Initials></Author><Author ValidYN="Y"><LastName>Slack</LastName><ForeName>Ruth S</ForeName><Initials>RS</Initials></Author><Author ValidYN="Y"><LastName>Mak</LastName><ForeName>Tak W</ForeName><Initials>TW</Initials></Author><Author ValidYN="Y"><LastName>Park</LastName><ForeName>David S</ForeName><Initials>DS</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>2010</Year><Month>01</Month><Day>26</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Proc Natl Acad Sci U S A</MedlineTA><NlmUniqueID>7505876</NlmUniqueID><ISSNLinking>0027-8424</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D009498">Neurotoxins</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D015513">Oncogene Proteins</NameOfSubstance></Chemical><Chemical><RegistryNumber>9P21XSP91P</RegistryNumber><NameOfSubstance UI="D015632">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</NameOfSubstance></Chemical><Chemical><RegistryNumber>BBX060AN9V</RegistryNumber><NameOfSubstance UI="D006861">Hydrogen 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Version="1">19254950</PMID></CommentsCorrections><CommentsCorrections RefType="Cites"><RefSource>Proc Natl Acad Sci U S A. 2007 Nov 20;104(47):18748-53</RefSource><PMID Version="1">18003894</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D015632" MajorTopicYN="N">1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000704" MajorTopicYN="N">Analysis of Variance</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015153" MajorTopicYN="N">Blotting, Western</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002458" MajorTopicYN="N">Cell Fractionation</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D002478" MajorTopicYN="N">Cells, 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