Selenoprotein T Exerts an Essential Oxidoreductase Activity That Protects Dopaminergic Neurons in Mouse Models of Parkinson's Disease
Identifieur interne : 000165 ( Main/Merge ); précédent : 000164; suivant : 000166Selenoprotein T Exerts an Essential Oxidoreductase Activity That Protects Dopaminergic Neurons in Mouse Models of Parkinson's Disease
Auteurs : Loubna Boukhzar ; Abdallah Hamieh ; Dorthe Cartier ; Yannick Tanguy ; Ifat Alsharif ; Matthieu Castex ; Arnaud Arabo ; Sana El Hajji ; Jean-Jacques Bonnet ; Mohammed Errami ; Anthony Falluel-Morel ; Abdeslam Chagraoui ; Isabelle Lihrmann ; Youssef AnouarSource :
- Antioxidants & Redox Signaling [ 1523-0864 ] ; 2016.
English descriptors
- KwdEn :
- Animals, Cell Death (drug effects), Disease Models, Animal, Dopaminergic Neurons (drug effects), Dopaminergic Neurons (metabolism), Mice, Mice, Inbred C57BL, Mice, Knockout, Neurotoxins (pharmacology), Oxidative Stress (drug effects), Oxidoreductases (metabolism), Parkinson Disease (metabolism), Parkinson Disease (pathology), Selenoproteins (deficiency), Selenoproteins (metabolism).
- MESH :
- chemical , deficiency : Selenoproteins.
- chemical , metabolism : Oxidoreductases, Selenoproteins.
- chemical , pharmacology : Neurotoxins.
- drug effects : Cell Death, Dopaminergic Neurons, Oxidative Stress.
- metabolism : Dopaminergic Neurons, Parkinson Disease.
- pathology : Parkinson Disease.
- Animals, Disease Models, Animal, Mice, Mice, Inbred C57BL, Mice, Knockout.
Abstract
Url:
DOI: 10.1089/ars.2015.6478
PubMed: 26866473
PubMed Central: 4840926
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PMC:4840926Le document en format XML
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<author><name sortKey="Errami, Mohammed" sort="Errami, Mohammed" uniqKey="Errami M" first="Mohammed" last="Errami">Mohammed Errami</name>
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<author><name sortKey="Lihrmann, Isabelle" sort="Lihrmann, Isabelle" uniqKey="Lihrmann I" first="Isabelle" last="Lihrmann">Isabelle Lihrmann</name>
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<author><name sortKey="Anouar, Youssef" sort="Anouar, Youssef" uniqKey="Anouar Y" first="Youssef" last="Anouar">Youssef Anouar</name>
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<series><title level="j">Antioxidants & Redox Signaling</title>
<idno type="ISSN">1523-0864</idno>
<idno type="eISSN">1557-7716</idno>
<imprint><date when="2016">2016</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term>
<term>Cell Death (drug effects)</term>
<term>Disease Models, Animal</term>
<term>Dopaminergic Neurons (drug effects)</term>
<term>Dopaminergic Neurons (metabolism)</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
<term>Neurotoxins (pharmacology)</term>
<term>Oxidative Stress (drug effects)</term>
<term>Oxidoreductases (metabolism)</term>
<term>Parkinson Disease (metabolism)</term>
<term>Parkinson Disease (pathology)</term>
<term>Selenoproteins (deficiency)</term>
<term>Selenoproteins (metabolism)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Selenoproteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Oxidoreductases</term>
<term>Selenoproteins</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Neurotoxins</term>
</keywords>
<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Death</term>
<term>Dopaminergic Neurons</term>
<term>Oxidative Stress</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Dopaminergic Neurons</term>
<term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Disease Models, Animal</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Mice, Knockout</term>
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<front><div type="abstract" xml:lang="en"><title>Abstract</title>
<p><bold><italic>Aims:</italic>
</bold>
Oxidative stress is central to the pathogenesis of Parkinson's disease (PD), but the mechanisms involved in the control of this stress in dopaminergic cells are not fully understood. There is increasing evidence that selenoproteins play a central role in the control of redox homeostasis and cell defense, but the precise contribution of members of this family of proteins during the course of neurodegenerative diseases is still elusive. <bold><italic>Results:</italic>
</bold>
We demonstrated first that selenoprotein T (SelT) whose gene disruption is lethal during embryogenesis, exerts a potent oxidoreductase activity. In the SH-SY5Y cell model of dopaminergic neurons, both silencing and overexpression of SelT affected oxidative stress and cell survival. Treatment with PD-inducing neurotoxins such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or rotenone triggered SelT expression in the nigrostriatal pathway of wild-type mice, but provoked rapid and severe parkinsonian-like motor defects in conditional brain SelT-deficient mice. This motor impairment was associated with marked oxidative stress and neurodegeneration and decreased tyrosine hydroxylase activity and dopamine levels in the nigrostriatal system. Finally, in PD patients, we report that SelT is tremendously increased in the caudate putamen tissue. <bold><italic>Innovation:</italic>
</bold>
These results reveal the activity of a novel selenoprotein enzyme that protects dopaminergic neurons against oxidative stress and prevents early and severe movement impairment in animal models of PD. <bold><italic>Conclusions:</italic>
</bold>
Our findings indicate that selenoproteins such as SelT play a crucial role in the protection of dopaminergic neurons against oxidative stress and cell death, providing insight into the molecular underpinnings of this stress in PD. <italic>Antioxid. Redox Signal.</italic>
24, 557–574.</p>
</div>
</front>
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