DJ-1 protects the nigrostriatal axis from the neurotoxin MPTP by modulation of the AKT pathway
Identifieur interne : 000C13 ( Ncbi/Checkpoint ); précédent : 000C12; suivant : 000C14DJ-1 protects the nigrostriatal axis from the neurotoxin MPTP by modulation of the AKT pathway
Auteurs : Hossein Aleyasin [Canada] ; Maxime W. C. Rousseaux [Canada] ; Paul C. Marcogliese [Canada] ; Sarah J. Hewitt [Canada] ; Isabella Irrcher [Canada] ; Alvin P. Joselin [Canada] ; Mohammad Parsanejad [Canada] ; Raymond H. Kim [Canada] ; Patrizia Rizzu [Pays-Bas] ; Steve M. Callaghan [Canada] ; Ruth S. Slack [Canada] ; Tak W. Mak [Canada] ; David S. Park [Canada, Corée du Sud]Source :
- Proceedings of the National Academy of Sciences of the United States of America [ 0027-8424 ] ; 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 H2O2 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.
Url:
DOI: 10.1073/pnas.0914876107
PubMed: 20133695
PubMed Central: 2840364
Affiliations:
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PMC:2840364Le document en format XML
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, Geumjeong GU, Busan 609 735<country>South Korea</country>
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, Van der Boechorststraat 7, 1081 BT, Amsterdam,<country>The Netherlands</country>
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;</nlm:aff>
<country xml:lang="fr">Canada</country>
<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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;</nlm:aff>
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;</nlm:aff>
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<wicri:regionArea># see nlm:aff country strict</wicri:regionArea>
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, Geumjeong GU, Busan 609 735<country>South Korea</country>
</nlm:aff>
<country xml:lang="fr">Corée du Sud</country>
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<term>Animals</term>
<term>Blotting, Western</term>
<term>Cell Fractionation</term>
<term>Cells, Cultured</term>
<term>Hydrogen Peroxide (metabolism)</term>
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<term>Mice</term>
<term>Neurons (metabolism)</term>
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<term>Protein Deglycase DJ-1</term>
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<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>
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<front><div type="abstract" xml:lang="en"><p>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<sub>2</sub>
O<sub>2</sub>
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.</p>
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<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>
<name sortKey="Slack, Ruth S" sort="Slack, Ruth S" uniqKey="Slack R" first="Ruth S." last="Slack">Ruth S. Slack</name>
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<country name="Pays-Bas"><noRegion><name sortKey="Rizzu, Patrizia" sort="Rizzu, Patrizia" uniqKey="Rizzu P" first="Patrizia" last="Rizzu">Patrizia Rizzu</name>
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<country name="Corée du Sud"><noRegion><name sortKey="Park, David S" sort="Park, David S" uniqKey="Park D" first="David S." last="Park">David S. Park</name>
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