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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">A role for mitogen- and stress-activated kinase 1 in L-DOPA-induced dyskinesia and ΔFosB expression</title><author><name sortKey="Feyder, Michael" sort="Feyder, Michael" uniqKey="Feyder M" first="Michael" last="Feyder">Michael Feyder</name><affiliation><nlm:aff id="A1">Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden</nlm:aff></affiliation></author><author><name sortKey="Sodersten, Erik" sort="Sodersten, Erik" uniqKey="Sodersten E" first="Erik" last="Södersten">Erik Södersten</name><affiliation><nlm:aff id="A1">Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Biotech Research and Innovation Centre (BRIC) and Centre for Epigenetics, University of Copenhagen, Copenhagen, Denmark</nlm:aff></affiliation></author><author><name sortKey="Santini, Emanuela" sort="Santini, Emanuela" uniqKey="Santini E" first="Emanuela" last="Santini">Emanuela Santini</name><affiliation><nlm:aff id="A1">Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden</nlm:aff></affiliation></author><author><name sortKey="Vialou, Vincent" sort="Vialou, Vincent" uniqKey="Vialou V" first="Vincent" last="Vialou">Vincent Vialou</name><affiliation><nlm:aff id="A3">Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029</nlm:aff></affiliation><affiliation><nlm:aff id="A4">INSERM, U952, CNRS UMR 7224, Université Pierre et Marie Curie, Paris 06, Paris, France</nlm:aff></affiliation></author><author><name sortKey="Laplant, Quincey C" sort="Laplant, Quincey C" uniqKey="Laplant Q" first="Quincey C." last="Laplant">Quincey C. Laplant</name><affiliation><nlm:aff id="A3">Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029</nlm:aff></affiliation></author><author><name sortKey="Watts, Emily L" sort="Watts, Emily L" uniqKey="Watts E" first="Emily L." last="Watts">Emily L. Watts</name><affiliation><nlm:aff id="A3">Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029</nlm:aff></affiliation></author><author><name sortKey="Spigolon, Giada" sort="Spigolon, Giada" uniqKey="Spigolon G" first="Giada" last="Spigolon">Giada Spigolon</name><affiliation><nlm:aff id="A1">Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden</nlm:aff></affiliation></author><author><name sortKey="Hansen, Klaus" sort="Hansen, Klaus" uniqKey="Hansen K" first="Klaus" last="Hansen">Klaus Hansen</name><affiliation><nlm:aff id="A2">Biotech Research and Innovation Centre (BRIC) and Centre for Epigenetics, University of Copenhagen, Copenhagen, Denmark</nlm:aff></affiliation></author><author><name sortKey="Caboche, Jocelyne" sort="Caboche, Jocelyne" uniqKey="Caboche J" first="Jocelyne" last="Caboche">Jocelyne Caboche</name><affiliation><nlm:aff id="A4">INSERM, U952, CNRS UMR 7224, Université Pierre et Marie Curie, Paris 06, Paris, France</nlm:aff></affiliation></author><author><name sortKey="Nestler, Eric" sort="Nestler, Eric" uniqKey="Nestler E" first="Eric" last="Nestler">Eric Nestler</name><affiliation><nlm:aff id="A3">Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029</nlm:aff></affiliation></author><author><name sortKey="Fisone, Gilberto" sort="Fisone, Gilberto" uniqKey="Fisone G" first="Gilberto" last="Fisone">Gilberto Fisone</name><affiliation><nlm:aff id="A1">Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden</nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">25193242</idno><idno type="pmc">4309747</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4309747</idno><idno type="RBID">PMC:4309747</idno><idno type="doi">10.1016/j.biopsych.2014.07.019</idno><date when="2014">2014</date><idno type="wicri:Area/Pmc/Corpus">000572</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000572</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">A role for mitogen- and stress-activated kinase 1 in L-DOPA-induced dyskinesia and ΔFosB expression</title><author><name sortKey="Feyder, Michael" sort="Feyder, Michael" uniqKey="Feyder M" first="Michael" last="Feyder">Michael Feyder</name><affiliation><nlm:aff id="A1">Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden</nlm:aff></affiliation></author><author><name sortKey="Sodersten, Erik" sort="Sodersten, Erik" uniqKey="Sodersten E" first="Erik" last="Södersten">Erik Södersten</name><affiliation><nlm:aff id="A1">Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden</nlm:aff></affiliation><affiliation><nlm:aff id="A2">Biotech Research and Innovation Centre (BRIC) and Centre for Epigenetics, University of Copenhagen, Copenhagen, Denmark</nlm:aff></affiliation></author><author><name sortKey="Santini, Emanuela" sort="Santini, Emanuela" uniqKey="Santini E" first="Emanuela" last="Santini">Emanuela Santini</name><affiliation><nlm:aff id="A1">Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden</nlm:aff></affiliation></author><author><name sortKey="Vialou, Vincent" sort="Vialou, Vincent" uniqKey="Vialou V" first="Vincent" last="Vialou">Vincent Vialou</name><affiliation><nlm:aff id="A3">Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029</nlm:aff></affiliation><affiliation><nlm:aff id="A4">INSERM, U952, CNRS UMR 7224, Université Pierre et Marie Curie, Paris 06, Paris, France</nlm:aff></affiliation></author><author><name sortKey="Laplant, Quincey C" sort="Laplant, Quincey C" uniqKey="Laplant Q" first="Quincey C." last="Laplant">Quincey C. Laplant</name><affiliation><nlm:aff id="A3">Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029</nlm:aff></affiliation></author><author><name sortKey="Watts, Emily L" sort="Watts, Emily L" uniqKey="Watts E" first="Emily L." last="Watts">Emily L. Watts</name><affiliation><nlm:aff id="A3">Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029</nlm:aff></affiliation></author><author><name sortKey="Spigolon, Giada" sort="Spigolon, Giada" uniqKey="Spigolon G" first="Giada" last="Spigolon">Giada Spigolon</name><affiliation><nlm:aff id="A1">Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden</nlm:aff></affiliation></author><author><name sortKey="Hansen, Klaus" sort="Hansen, Klaus" uniqKey="Hansen K" first="Klaus" last="Hansen">Klaus Hansen</name><affiliation><nlm:aff id="A2">Biotech Research and Innovation Centre (BRIC) and Centre for Epigenetics, University of Copenhagen, Copenhagen, Denmark</nlm:aff></affiliation></author><author><name sortKey="Caboche, Jocelyne" sort="Caboche, Jocelyne" uniqKey="Caboche J" first="Jocelyne" last="Caboche">Jocelyne Caboche</name><affiliation><nlm:aff id="A4">INSERM, U952, CNRS UMR 7224, Université Pierre et Marie Curie, Paris 06, Paris, France</nlm:aff></affiliation></author><author><name sortKey="Nestler, Eric" sort="Nestler, Eric" uniqKey="Nestler E" first="Eric" last="Nestler">Eric Nestler</name><affiliation><nlm:aff id="A3">Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029</nlm:aff></affiliation></author><author><name sortKey="Fisone, Gilberto" sort="Fisone, Gilberto" uniqKey="Fisone G" first="Gilberto" last="Fisone">Gilberto Fisone</name><affiliation><nlm:aff id="A1">Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden</nlm:aff></affiliation></author></analytic><series><title level="j">Biological psychiatry</title><idno type="ISSN">0006-3223</idno><idno type="eISSN">1873-2402</idno><imprint><date when="2014">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Background</title><p id="P1">Abnormal regulation of extracellular signal-regulated kinases 1 and 2 (ERK) has been implicated in L-DOPA-induced dyskinesia (LID), a motor complication affecting Parkinson’s disease (PD) patients subjected to standard pharmacotherapy. We examined the involvement in LID of the mitogen- and stress-activated kinase 1 (MSK1), a downstream target of ERK and an important regulator of transcription.</p></sec><sec id="S2"><title>Methods</title><p id="P2">MSK1 knockout (MSK1 KO) mice and ΔFosB- or ΔcJun-overexpressing transgenic mice were lesioned with 6-hydroxydopamine to produce a model of PD and assessed for LID following chronic L-DOPA administration. Biochemical processes were evaluated by Western blotting or immunoflourescence. Histone H3 phosphorylation was analyzed by chromatin immunoprecipitation (ChIP) followed by promotor-specific quantitative PCR.</p></sec><sec id="S3"><title>Results</title><p id="P3">Genetic inactivation of MSK1 attenuated LID and reduced the phosphorylation of histone H3 at Ser10 in the striatum. ChIP analysis showed that this reduction occurred at the level of the <italic>fosB</italic> gene promoter. In line with this observation, the accumulation of ΔFosB produced by chronic L-DOPA was reduced in MSK1 KO. Moreover, inducible overexpression of ΔFosB in striatonigral medium spiny neurons exacerbated dyskinetic behavior, whereas overexpression of ΔcJun, which reduces ΔFosB-dependent transcriptional activation, counteracted LID.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">These results indicate that abnormal regulation of MSK1 contributes to the development of LID and to the concomitant increase in striatal ΔFosB, which may occur via increased histone H3 phosphorylation at the <italic>fosB</italic> promoter. They also show that accumulation of ΔFosB in striatonigral neurons is causally related to the development of dyskinesia.</p></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<pmc-dir>properties manuscript</pmc-dir>
<front><journal-meta><journal-id journal-id-type="nlm-journal-id">0213264</journal-id><journal-id journal-id-type="pubmed-jr-id">1117</journal-id><journal-id journal-id-type="nlm-ta">Biol Psychiatry</journal-id><journal-id journal-id-type="iso-abbrev">Biol. Psychiatry</journal-id><journal-title-group><journal-title>Biological psychiatry</journal-title></journal-title-group><issn pub-type="ppub">0006-3223</issn><issn pub-type="epub">1873-2402</issn></journal-meta><article-meta><article-id pub-id-type="pmid">25193242</article-id><article-id pub-id-type="pmc">4309747</article-id><article-id pub-id-type="doi">10.1016/j.biopsych.2014.07.019</article-id><article-id pub-id-type="manuscript">NIHMS639852</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>A role for mitogen- and stress-activated kinase 1 in L-DOPA-induced dyskinesia and ΔFosB expression</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Feyder</surname><given-names>Michael</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Södersten</surname><given-names>Erik</given-names></name><xref ref-type="aff" rid="A1">1</xref><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Santini</surname><given-names>Emanuela</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Vialou</surname><given-names>Vincent</given-names></name><xref ref-type="aff" rid="A3">3</xref><xref ref-type="aff" rid="A4">4</xref></contrib><contrib contrib-type="author"><name><surname>LaPlant</surname><given-names>Quincey C.</given-names></name><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Watts</surname><given-names>Emily L.</given-names></name><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Spigolon</surname><given-names>Giada</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib><contrib contrib-type="author"><name><surname>Hansen</surname><given-names>Klaus</given-names></name><xref ref-type="aff" rid="A2">2</xref></contrib><contrib contrib-type="author"><name><surname>Caboche</surname><given-names>Jocelyne</given-names></name><xref ref-type="aff" rid="A4">4</xref></contrib><contrib contrib-type="author"><name><surname>Nestler</surname><given-names>Eric</given-names></name><xref ref-type="aff" rid="A3">3</xref></contrib><contrib contrib-type="author"><name><surname>Fisone</surname><given-names>Gilberto</given-names></name><xref ref-type="aff" rid="A1">1</xref></contrib></contrib-group><aff id="A1"><label>1</label>Department of Neuroscience, Karolinska Institutet, 171 77 Stockholm, Sweden</aff><aff id="A2"><label>2</label>Biotech Research and Innovation Centre (BRIC) and Centre for Epigenetics, University of Copenhagen, Copenhagen, Denmark</aff><aff id="A3"><label>3</label>Fishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, New York 10029</aff><aff id="A4"><label>4</label>INSERM, U952, CNRS UMR 7224, Université Pierre et Marie Curie, Paris 06, Paris, France</aff><author-notes><corresp id="FN1">Corresponding author: Gilberto Fisone, Department of Neuroscience, Karolinska Institutet, Retzius väg 8, 171 77 Stockholm, Sweden, Phone: +46-8-52487375, Fax: +46-8-320988, <email>gilberto.fisone@ki.se</email></corresp></author-notes><pub-date pub-type="nihms-submitted"><day>4</day><month>11</month><year>2014</year></pub-date><pub-date pub-type="epub"><day>28</day><month>7</month><year>2014</year></pub-date><pub-date pub-type="ppub"><day>1</day><month>3</month><year>2016</year></pub-date><pub-date pub-type="pmc-release"><day>01</day><month>9</month><year>2016</year></pub-date><volume>79</volume><issue>5</issue><fpage>362</fpage><lpage>371</lpage><pmc-comment>elocation-id from pubmed: 10.1016/j.biopsych.2014.07.019</pmc-comment>
<abstract><sec id="S1"><title>Background</title><p id="P1">Abnormal regulation of extracellular signal-regulated kinases 1 and 2 (ERK) has been implicated in L-DOPA-induced dyskinesia (LID), a motor complication affecting Parkinson’s disease (PD) patients subjected to standard pharmacotherapy. We examined the involvement in LID of the mitogen- and stress-activated kinase 1 (MSK1), a downstream target of ERK and an important regulator of transcription.</p></sec><sec id="S2"><title>Methods</title><p id="P2">MSK1 knockout (MSK1 KO) mice and ΔFosB- or ΔcJun-overexpressing transgenic mice were lesioned with 6-hydroxydopamine to produce a model of PD and assessed for LID following chronic L-DOPA administration. Biochemical processes were evaluated by Western blotting or immunoflourescence. Histone H3 phosphorylation was analyzed by chromatin immunoprecipitation (ChIP) followed by promotor-specific quantitative PCR.</p></sec><sec id="S3"><title>Results</title><p id="P3">Genetic inactivation of MSK1 attenuated LID and reduced the phosphorylation of histone H3 at Ser10 in the striatum. ChIP analysis showed that this reduction occurred at the level of the <italic>fosB</italic> gene promoter. In line with this observation, the accumulation of ΔFosB produced by chronic L-DOPA was reduced in MSK1 KO. Moreover, inducible overexpression of ΔFosB in striatonigral medium spiny neurons exacerbated dyskinetic behavior, whereas overexpression of ΔcJun, which reduces ΔFosB-dependent transcriptional activation, counteracted LID.</p></sec><sec id="S4"><title>Conclusions</title><p id="P4">These results indicate that abnormal regulation of MSK1 contributes to the development of LID and to the concomitant increase in striatal ΔFosB, which may occur via increased histone H3 phosphorylation at the <italic>fosB</italic> promoter. They also show that accumulation of ΔFosB in striatonigral neurons is causally related to the development of dyskinesia.</p></sec></abstract><kwd-group><kwd>Parkinson’s disease</kwd><kwd>dopamine D1 receptor</kwd><kwd>histone</kwd><kwd>mouse</kwd><kwd>striatum</kwd><kwd>medium spiny neurons</kwd></kwd-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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