Rgs6 is Required for Adult Maintenance of Dopaminergic Neurons in the Ventral Substantia Nigra
Identifieur interne : 001A01 ( Ncbi/Curation ); précédent : 001A00; suivant : 001A02Rgs6 is Required for Adult Maintenance of Dopaminergic Neurons in the Ventral Substantia Nigra
Auteurs : Panojot Bifsha [Canada] ; Jianqi Yang [États-Unis] ; Rory A. Fisher [États-Unis] ; Jacques Drouin [Canada]Source :
- PLoS Genetics [ 1553-7390 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Dopaminergic Neurons (physiology), Homeodomain Proteins (metabolism), Mice, Inbred C57BL, Mice, Knockout, Organ Specificity, Parkinson Disease (genetics), Parkinson Disease (pathology), RGS Proteins (physiology), Signal Transduction, Substantia Nigra (pathology), Transcription Factors (metabolism).
- MESH :
- chemical , metabolism : Homeodomain Proteins, Transcription Factors.
- genetics : Parkinson Disease.
- pathology : Parkinson Disease, Substantia Nigra.
- physiology : Dopaminergic Neurons, RGS Proteins.
- Animals, Mice, Inbred C57BL, Mice, Knockout, Organ Specificity, Signal Transduction.
Abstract
Parkinson disease (PD) is characterized by the preferential, but poorly understood, vulnerability to degeneration of midbrain dopaminergic (mDA) neurons in the ventral substantia nigra compacta (vSNc). These sensitive mDA neurons express Pitx3, a transcription factor that is critical for their survival during development. We used this dependence to identify, by flow cytometry and expression profiling, the negative regulator of G-protein signaling Rgs6 for its restricted expression in these neurons. In contrast to
Url:
DOI: 10.1371/journal.pgen.1004863
PubMed: 25501001
PubMed Central: 4263397
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PMC:4263397Le document en format XML
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Fisher</name><affiliation wicri:level="2"><nlm:aff id="aff3"><addr-line>Department of Pharmacology, University of Iowa Carver College of Medicine, Iowa City, Iowa, United States of America</addr-line></nlm:aff><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Pharmacology, University of Iowa Carver College of Medicine, Iowa City, Iowa</wicri:regionArea><placeName><region type="state">Iowa</region></placeName></affiliation></author><author><name sortKey="Drouin, Jacques" sort="Drouin, Jacques" uniqKey="Drouin J" first="Jacques" last="Drouin">Jacques Drouin</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Laboratoire de Génétique Moléculaire, Institut de Recherches Cliniques de Montréal (IRCM) Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Laboratoire de Génétique Moléculaire, Institut de Recherches Cliniques de Montréal (IRCM) Montréal, Quebec</wicri:regionArea><wicri:noRegion>Quebec</wicri:noRegion></affiliation><affiliation wicri:level="4"><nlm:aff id="aff2"><addr-line>Division of Experimental Medicine, McGill University, Montréal, Quebec, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Experimental Medicine, McGill University, Montréal, Quebec</wicri:regionArea><orgName type="university">Université McGill</orgName><placeName><settlement type="city">Montréal</settlement><region type="state">Québec</region></placeName></affiliation></author></analytic><series><title level="j">PLoS Genetics</title><idno type="ISSN">1553-7390</idno><idno type="eISSN">1553-7404</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Dopaminergic Neurons (physiology)</term><term>Homeodomain Proteins (metabolism)</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Organ Specificity</term><term>Parkinson Disease (genetics)</term><term>Parkinson Disease (pathology)</term><term>RGS Proteins (physiology)</term><term>Signal Transduction</term><term>Substantia Nigra (pathology)</term><term>Transcription Factors (metabolism)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Homeodomain Proteins</term><term>Transcription Factors</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Parkinson Disease</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Dopaminergic Neurons</term><term>RGS Proteins</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Mice, Inbred C57BL</term><term>Mice, Knockout</term><term>Organ Specificity</term><term>Signal Transduction</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Parkinson disease (PD) is characterized by the preferential, but poorly understood, vulnerability to degeneration of midbrain dopaminergic (mDA) neurons in the ventral substantia nigra compacta (vSNc). These sensitive mDA neurons express Pitx3, a transcription factor that is critical for their survival during development. We used this dependence to identify, by flow cytometry and expression profiling, the negative regulator of G-protein signaling Rgs6 for its restricted expression in these neurons. In contrast to <italic>Pitx3<sup>−/−</sup></italic> mDA neurons that die during fetal (vSNc) or post-natal (VTA) period, the vSNc mDA neurons of <italic>Rgs6</italic><sup>−/−</sup> mutant mice begin to exhibit unilateral signs of degeneration at around 6 months of age, and by one year cell loss is observed in a fraction of mice. Unilateral cell loss is accompanied by contralateral degenerating neurons that exhibit smaller cell size, altered morphology and reduced dendritic network. The degenerating neurons have low levels of tyrosine hydroxylase (TH) and decreased nuclear Pitx3; accordingly, expression of many Pitx3 target gene products is altered, including Vmat2, Bdnf, Aldh1a1 (Adh2) and Fgf10. These low TH neurons also express markers of increased dopamine signaling, namely increased DAT and phospho-Erk1/2 expression. The late onset degeneration may reflect the protective action of Rgs6 against excessive DA signaling throughout life. Rgs6-dependent protection is thus critical for adult survival and maintenance of the vSNc mDA neurons that are most affected in PD.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Jellinger, Ka" uniqKey="Jellinger K">KA Jellinger</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Gonzalez Hernandez, T" uniqKey="Gonzalez Hernandez T">T Gonzalez-Hernandez</name></author><author><name sortKey="Cruz Muros, I" uniqKey="Cruz Muros I">I Cruz-Muros</name></author><author><name sortKey="Afonso Oramas, D" uniqKey="Afonso Oramas D">D Afonso-Oramas</name></author><author><name sortKey="Salas Hernandez, J" uniqKey="Salas Hernandez J">J Salas-Hernandez</name></author><author><name sortKey="Castro Hernandez, J" uniqKey="Castro Hernandez J">J Castro-Hernandez</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="Obeso, Ja" uniqKey="Obeso J">JA Obeso</name></author><author><name 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Takahashi</name></author></analytic></biblStruct><biblStruct><analytic><author><name sortKey="L Honore, A" uniqKey="L Honore A">A L'Honoré</name></author><author><name sortKey="Coulon, V" uniqKey="Coulon V">V Coulon</name></author><author><name sortKey="Marcil, A" uniqKey="Marcil A">A Marcil</name></author><author><name sortKey="Lebel, M" uniqKey="Lebel M">M Lebel</name></author><author><name sortKey="Lafrance Vanasse, J" uniqKey="Lafrance Vanasse J">J Lafrance-Vanasse</name></author></analytic></biblStruct></listBibl></div1></back></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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