α-Synuclein expression is induced by depolarization and cyclic AMP in enteric neurons
Identifieur interne : 000E59 ( PascalFrancis/Curation ); précédent : 000E58; suivant : 000E60α-Synuclein expression is induced by depolarization and cyclic AMP in enteric neurons
Auteurs : Sébastien Paillusson [France] ; Maddalena Tasselli [France] ; Thibaud Lebouvier [France] ; Maxime Michaël Mahe [France] ; Julien Chevalier [France] ; Mandy Biraud [France] ; Chystelle Cario-Toumaniantz [France] ; Michel Neunlist [France] ; Pascal Derkinderen [France]Source :
- Journal of neurochemistry [ 0022-3042 ] ; 2010.
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Abstract
Accumulated evidence emphasizes the importance of α-synuclein expression levels in Parkinson's disease (PD) pathogenesis. PD is a multicentric disorder that affects the enteric nervous system (ENS), whose involvement may herald the degenerative process in the CNS. We therefore undertook the present study to investigate the mechanisms involved in the regulation of expression of α-synuclein in the ENS. The regulation of α-synuclein expression was assessed by qPCR and western blot analysis in rat primary culture of ENS treated with KCI and forskolin. A pharmacological approach was used to decipher the signaling pathways involved. Intraperitoneal injections of Bay K-8644 and forskolin were performed in mice, whose proximal colons were further analyzed for α-synuclein expression. Depolarization and forskolin increased α-synuclein mRNA and protein expression in primary cultures of ENS, although L-type calcium channel and protein kinase A, respectively. Both stimuli increased α-synuclein expression through a Ras/extracellular signal-regulated kinases pathway. An increase in α-synuclein expression was also observed in vivo in the ENS of mice injected with Bay K-8644 or forskolin. In conclusion, we have identified stimuli leading to α-synuclein over-expression in the ENS, which could be critical in the initiation of the pathological process in PD.
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Neurology</s1><s2>Nantes</s2><s3>FRA</s3><sZ>3 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Michael Mahe, Maxime" sort="Michael Mahe, Maxime" uniqKey="Michael Mahe M" first="Maxime" last="Michaël Mahe">Maxime Michaël Mahe</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Inserm, U913</s1><s2>Nantes</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>University Nantes</s1><s2>Nantes</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Chevalier, Julien" sort="Chevalier, Julien" uniqKey="Chevalier J" first="Julien" last="Chevalier">Julien Chevalier</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Inserm, U913</s1><s2>Nantes</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Biraud, Mandy" sort="Biraud, Mandy" uniqKey="Biraud M" first="Mandy" last="Biraud">Mandy Biraud</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Inserm, U913</s1><s2>Nantes</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Cario Toumaniantz, Chystelle" sort="Cario Toumaniantz, Chystelle" uniqKey="Cario Toumaniantz C" first="Chystelle" last="Cario-Toumaniantz">Chystelle Cario-Toumaniantz</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>University Nantes</s1><s2>Nantes</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Inserm, U915</s1><s2>Nantes</s2><s3>FRA</s3><sZ>7 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Neunlist, Michel" sort="Neunlist, Michel" uniqKey="Neunlist M" first="Michel" last="Neunlist">Michel Neunlist</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Inserm, U913</s1><s2>Nantes</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>University Nantes</s1><s2>Nantes</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country></affiliation></author><author><name sortKey="Derkinderen, Pascal" sort="Derkinderen, Pascal" uniqKey="Derkinderen P" first="Pascal" last="Derkinderen">Pascal Derkinderen</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Inserm, U913</s1><s2>Nantes</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>University Nantes</s1><s2>Nantes</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country></affiliation><affiliation wicri:level="1"><inist:fA14 i1="03"><s1>CHU Nantes, Department of Neurology</s1><s2>Nantes</s2><s3>FRA</s3><sZ>3 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>France</country></affiliation></author></analytic><series><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno><imprint><date when="2010">2010</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neurochemistry</title><title level="j" type="abbreviated">J. neurochem.</title><idno type="ISSN">0022-3042</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Central nervous system</term><term>Colon</term><term>Cyclic AMP</term><term>Depolarization</term><term>Enteric nervous system</term><term>L-type calcium channel</term><term>Mouse</term><term>Neuron</term><term>Non-specific serine/threonine protein kinase</term><term>Parkinson disease</term><term>Pathogenesis</term><term>Primary culture</term><term>Protein</term><term>Rat</term><term>Signal transduction</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Dépolarisation</term><term>AMP cyclique</term><term>Neurone</term><term>Pathogénie</term><term>Système nerveux entérique</term><term>Système nerveux central</term><term>Culture primaire</term><term>Transduction signal</term><term>Maladie de Parkinson</term><term>Côlon</term><term>Protéine</term><term>Canal calcique L</term><term>Non-specific serine/threonine protein kinase</term><term>Rat</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Accumulated evidence emphasizes the importance of α-synuclein expression levels in Parkinson's disease (PD) pathogenesis. PD is a multicentric disorder that affects the enteric nervous system (ENS), whose involvement may herald the degenerative process in the CNS. We therefore undertook the present study to investigate the mechanisms involved in the regulation of expression of α-synuclein in the ENS. The regulation of α-synuclein expression was assessed by qPCR and western blot analysis in rat primary culture of ENS treated with KCI and forskolin. A pharmacological approach was used to decipher the signaling pathways involved. Intraperitoneal injections of Bay K-8644 and forskolin were performed in mice, whose proximal colons were further analyzed for α-synuclein expression. Depolarization and forskolin increased α-synuclein mRNA and protein expression in primary cultures of ENS, although L-type calcium channel and protein kinase A, respectively. Both stimuli increased α-synuclein expression through a Ras/extracellular signal-regulated kinases pathway. An increase in α-synuclein expression was also observed in vivo in the ENS of mice injected with Bay K-8644 or forskolin. In conclusion, we have identified stimuli leading to α-synuclein over-expression in the ENS, which could be critical in the initiation of the pathological process in PD.</div></front></TEI><inist><standard h6="B"><pA><fA01 i1="01" i2="1"><s0>0022-3042</s0></fA01><fA02 i1="01"><s0>JONRA9</s0></fA02><fA03 i2="1"><s0>J. neurochem.</s0></fA03><fA05><s2>115</s2></fA05><fA06><s2>3</s2></fA06><fA08 i1="01" i2="1" l="ENG"><s1>α-Synuclein expression is induced by depolarization and cyclic AMP in enteric neurons</s1></fA08><fA11 i1="01" i2="1"><s1>PAILLUSSON (Sébastien)</s1></fA11><fA11 i1="02" i2="1"><s1>TASSELLI (Maddalena)</s1></fA11><fA11 i1="03" i2="1"><s1>LEBOUVIER (Thibaud)</s1></fA11><fA11 i1="04" i2="1"><s1>MICHAËL MAHE (Maxime)</s1></fA11><fA11 i1="05" i2="1"><s1>CHEVALIER (Julien)</s1></fA11><fA11 i1="06" i2="1"><s1>BIRAUD (Mandy)</s1></fA11><fA11 i1="07" i2="1"><s1>CARIO-TOUMANIANTZ (Chystelle)</s1></fA11><fA11 i1="08" i2="1"><s1>NEUNLIST (Michel)</s1></fA11><fA11 i1="09" i2="1"><s1>DERKINDEREN (Pascal)</s1></fA11><fA14 i1="01"><s1>Inserm, U913</s1><s2>Nantes</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></fA14><fA14 i1="02"><s1>University Nantes</s1><s2>Nantes</s2><s3>FRA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>3 aut.</sZ><sZ>4 aut.</sZ><sZ>7 aut.</sZ><sZ>8 aut.</sZ><sZ>9 aut.</sZ></fA14><fA14 i1="03"><s1>CHU Nantes, Department of Neurology</s1><s2>Nantes</s2><s3>FRA</s3><sZ>3 aut.</sZ><sZ>9 aut.</sZ></fA14><fA14 i1="04"><s1>Inserm, U915</s1><s2>Nantes</s2><s3>FRA</s3><sZ>7 aut.</sZ></fA14><fA20><s1>694-706</s1></fA20><fA21><s1>2010</s1></fA21><fA23 i1="01"><s0>ENG</s0></fA23><fA43 i1="01"><s1>INIST</s1><s2>4037</s2><s5>354000192772850150</s5></fA43><fA44><s0>0000</s0><s1>© 2010 INIST-CNRS. All rights reserved.</s1></fA44><fA45><s0>1 p.1/4</s0></fA45><fA47 i1="01" i2="1"><s0>10-0488417</s0></fA47><fA60><s1>P</s1></fA60><fA61><s0>A</s0></fA61><fA64 i1="01" i2="1"><s0>Journal of neurochemistry</s0></fA64><fA66 i1="01"><s0>GBR</s0></fA66><fC01 i1="01" l="ENG"><s0>Accumulated evidence emphasizes the importance of α-synuclein expression levels in Parkinson's disease (PD) pathogenesis. PD is a multicentric disorder that affects the enteric nervous system (ENS), whose involvement may herald the degenerative process in the CNS. We therefore undertook the present study to investigate the mechanisms involved in the regulation of expression of α-synuclein in the ENS. The regulation of α-synuclein expression was assessed by qPCR and western blot analysis in rat primary culture of ENS treated with KCI and forskolin. A pharmacological approach was used to decipher the signaling pathways involved. Intraperitoneal injections of Bay K-8644 and forskolin were performed in mice, whose proximal colons were further analyzed for α-synuclein expression. Depolarization and forskolin increased α-synuclein mRNA and protein expression in primary cultures of ENS, although L-type calcium channel and protein kinase A, respectively. Both stimuli increased α-synuclein expression through a Ras/extracellular signal-regulated kinases pathway. An increase in α-synuclein expression was also observed in vivo in the ENS of mice injected with Bay K-8644 or forskolin. In conclusion, we have identified stimuli leading to α-synuclein over-expression in the ENS, which could be critical in the initiation of the pathological process in PD.</s0></fC01><fC02 i1="01" i2="X"><s0>002B17G</s0></fC02><fC02 i1="02" i2="X"><s0>002B17A01</s0></fC02><fC03 i1="01" i2="X" l="FRE"><s0>Dépolarisation</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="ENG"><s0>Depolarization</s0><s5>01</s5></fC03><fC03 i1="01" i2="X" l="SPA"><s0>Despolarización</s0><s5>01</s5></fC03><fC03 i1="02" i2="X" l="FRE"><s0>AMP cyclique</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="ENG"><s0>Cyclic AMP</s0><s5>02</s5></fC03><fC03 i1="02" i2="X" l="SPA"><s0>AMP cíclico</s0><s5>02</s5></fC03><fC03 i1="03" i2="X" l="FRE"><s0>Neurone</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="ENG"><s0>Neuron</s0><s5>03</s5></fC03><fC03 i1="03" i2="X" l="SPA"><s0>Neurona</s0><s5>03</s5></fC03><fC03 i1="04" i2="X" l="FRE"><s0>Pathogénie</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="ENG"><s0>Pathogenesis</s0><s5>04</s5></fC03><fC03 i1="04" i2="X" l="SPA"><s0>Patogenia</s0><s5>04</s5></fC03><fC03 i1="05" i2="X" l="FRE"><s0>Système nerveux entérique</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="ENG"><s0>Enteric nervous system</s0><s5>05</s5></fC03><fC03 i1="05" i2="X" l="SPA"><s0>Sistema nervioso entérico</s0><s5>05</s5></fC03><fC03 i1="06" i2="X" l="FRE"><s0>Système nerveux central</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="ENG"><s0>Central nervous system</s0><s5>06</s5></fC03><fC03 i1="06" i2="X" l="SPA"><s0>Sistema nervioso central</s0><s5>06</s5></fC03><fC03 i1="07" i2="X" l="FRE"><s0>Culture primaire</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="ENG"><s0>Primary culture</s0><s5>07</s5></fC03><fC03 i1="07" i2="X" l="SPA"><s0>Cultivo primario</s0><s5>07</s5></fC03><fC03 i1="08" i2="X" l="FRE"><s0>Transduction signal</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="ENG"><s0>Signal transduction</s0><s5>08</s5></fC03><fC03 i1="08" i2="X" l="SPA"><s0>Transducción señal</s0><s5>08</s5></fC03><fC03 i1="09" i2="X" l="FRE"><s0>Maladie de Parkinson</s0><s2>NM</s2><s5>09</s5></fC03><fC03 i1="09" i2="X" l="ENG"><s0>Parkinson disease</s0><s2>NM</s2><s5>09</s5></fC03><fC03 i1="09" i2="X" l="SPA"><s0>Parkinson enfermedad</s0><s2>NM</s2><s5>09</s5></fC03><fC03 i1="10" i2="X" l="FRE"><s0>Côlon</s0><s5>10</s5></fC03><fC03 i1="10" i2="X" l="ENG"><s0>Colon</s0><s5>10</s5></fC03><fC03 i1="10" i2="X" l="SPA"><s0>Colón</s0><s5>10</s5></fC03><fC03 i1="11" i2="X" l="FRE"><s0>Protéine</s0><s5>11</s5></fC03><fC03 i1="11" i2="X" l="ENG"><s0>Protein</s0><s5>11</s5></fC03><fC03 i1="11" i2="X" l="SPA"><s0>Proteína</s0><s5>11</s5></fC03><fC03 i1="12" i2="X" l="FRE"><s0>Canal calcique L</s0><s5>13</s5></fC03><fC03 i1="12" i2="X" l="ENG"><s0>L-type calcium channel</s0><s5>13</s5></fC03><fC03 i1="12" i2="X" l="SPA"><s0>Canal calcio tipo L</s0><s5>13</s5></fC03><fC03 i1="13" i2="X" l="FRE"><s0>Non-specific serine/threonine protein kinase</s0><s2>FE</s2><s5>14</s5></fC03><fC03 i1="13" i2="X" l="ENG"><s0>Non-specific serine/threonine protein kinase</s0><s2>FE</s2><s5>14</s5></fC03><fC03 i1="13" i2="X" l="SPA"><s0>Non-specific serine/threonine protein kinase</s0><s2>FE</s2><s5>14</s5></fC03><fC03 i1="14" i2="X" l="FRE"><s0>Rat</s0><s5>54</s5></fC03><fC03 i1="14" i2="X" l="ENG"><s0>Rat</s0><s5>54</s5></fC03><fC03 i1="14" i2="X" l="SPA"><s0>Rata</s0><s5>54</s5></fC03><fC03 i1="15" i2="X" l="FRE"><s0>Souris</s0><s5>55</s5></fC03><fC03 i1="15" i2="X" l="ENG"><s0>Mouse</s0><s5>55</s5></fC03><fC03 i1="15" i2="X" l="SPA"><s0>Ratón</s0><s5>55</s5></fC03><fC07 i1="01" i2="X" l="FRE"><s0>Transferases</s0><s2>FE</s2></fC07><fC07 i1="01" i2="X" l="ENG"><s0>Transferases</s0><s2>FE</s2></fC07><fC07 i1="01" i2="X" l="SPA"><s0>Transferases</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="FRE"><s0>Enzyme</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="ENG"><s0>Enzyme</s0><s2>FE</s2></fC07><fC07 i1="02" i2="X" l="SPA"><s0>Enzima</s0><s2>FE</s2></fC07><fC07 i1="03" i2="X" l="FRE"><s0>Pathologie de l'encéphale</s0><s5>20</s5></fC07><fC07 i1="03" i2="X" l="ENG"><s0>Cerebral disorder</s0><s5>20</s5></fC07><fC07 i1="03" i2="X" l="SPA"><s0>Encéfalo patología</s0><s5>20</s5></fC07><fC07 i1="04" i2="X" l="FRE"><s0>Syndrome extrapyramidal</s0><s5>21</s5></fC07><fC07 i1="04" i2="X" l="ENG"><s0>Extrapyramidal syndrome</s0><s5>21</s5></fC07><fC07 i1="04" i2="X" l="SPA"><s0>Extrapiramidal síndrome</s0><s5>21</s5></fC07><fC07 i1="05" i2="X" l="FRE"><s0>Maladie dégénérative</s0><s5>22</s5></fC07><fC07 i1="05" i2="X" l="ENG"><s0>Degenerative disease</s0><s5>22</s5></fC07><fC07 i1="05" i2="X" l="SPA"><s0>Enfermedad degenerativa</s0><s5>22</s5></fC07><fC07 i1="06" i2="X" l="FRE"><s0>Pathologie du système nerveux central</s0><s5>23</s5></fC07><fC07 i1="06" i2="X" l="ENG"><s0>Central nervous system disease</s0><s5>23</s5></fC07><fC07 i1="06" i2="X" l="SPA"><s0>Sistema nervosio central patología</s0><s5>23</s5></fC07><fC07 i1="07" i2="X" l="FRE"><s0>Pathologie du système nerveux</s0><s5>24</s5></fC07><fC07 i1="07" i2="X" l="ENG"><s0>Nervous system diseases</s0><s5>24</s5></fC07><fC07 i1="07" i2="X" l="SPA"><s0>Sistema nervioso patología</s0><s5>24</s5></fC07><fC07 i1="08" i2="X" l="FRE"><s0>Appareil digestif</s0><s5>25</s5></fC07><fC07 i1="08" i2="X" l="ENG"><s0>Digestive system</s0><s5>25</s5></fC07><fC07 i1="08" i2="X" l="SPA"><s0>Aparato digestivo</s0><s5>25</s5></fC07><fC07 i1="09" i2="X" l="FRE"><s0>Intestin</s0><s5>26</s5></fC07><fC07 i1="09" i2="X" l="ENG"><s0>Gut</s0><s5>26</s5></fC07><fC07 i1="09" i2="X" l="SPA"><s0>Intestino</s0><s5>26</s5></fC07><fC07 i1="10" i2="X" l="FRE"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="10" i2="X" l="ENG"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="10" i2="X" l="SPA"><s0>Rodentia</s0><s2>NS</s2></fC07><fC07 i1="11" i2="X" l="FRE"><s0>Mammalia</s0><s2>NS</s2></fC07><fC07 i1="11" i2="X" 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