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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Acceleration in the Rate of CNS Remyelination in Lysolecithin-Induced Demyelination</title><author><name sortKey="Pavelko, Kevin D" sort="Pavelko, Kevin D" uniqKey="Pavelko K" first="Kevin D." last="Pavelko">Kevin D. Pavelko</name><affiliation><nlm:aff id="tO1"></nlm:aff></affiliation></author><author><name sortKey="Van Engelen, Baziel G M" sort="Van Engelen, Baziel G M" uniqKey="Van Engelen B" first="Baziel G. M." last="Van Engelen">Baziel G. M. Van Engelen</name><affiliation><nlm:aff id="tO1"></nlm:aff></affiliation><affiliation><nlm:aff id="tO2"></nlm:aff></affiliation></author><author><name sortKey="Rodriguez, Moses" sort="Rodriguez, Moses" uniqKey="Rodriguez M" first="Moses" last="Rodriguez">Moses Rodriguez</name><affiliation><nlm:aff id="tO1"></nlm:aff></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">9502810</idno><idno type="pmc">6793082</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6793082</idno><idno type="RBID">PMC:6793082</idno><idno type="doi">10.1523/JNEUROSCI.18-07-02498.1998</idno><date when="1998">1998</date><idno type="wicri:Area/Pmc/Corpus">000708</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000708</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Acceleration in the Rate of CNS Remyelination in Lysolecithin-Induced Demyelination</title><author><name sortKey="Pavelko, Kevin D" sort="Pavelko, Kevin D" uniqKey="Pavelko K" first="Kevin D." last="Pavelko">Kevin D. Pavelko</name><affiliation><nlm:aff id="tO1"></nlm:aff></affiliation></author><author><name sortKey="Van Engelen, Baziel G M" sort="Van Engelen, Baziel G M" uniqKey="Van Engelen B" first="Baziel G. M." last="Van Engelen">Baziel G. M. Van Engelen</name><affiliation><nlm:aff id="tO1"></nlm:aff></affiliation><affiliation><nlm:aff id="tO2"></nlm:aff></affiliation></author><author><name sortKey="Rodriguez, Moses" sort="Rodriguez, Moses" uniqKey="Rodriguez M" first="Moses" last="Rodriguez">Moses Rodriguez</name><affiliation><nlm:aff id="tO1"></nlm:aff></affiliation></author></analytic><series><title level="j">The Journal of Neuroscience</title><idno type="ISSN">0270-6474</idno><idno type="eISSN">1529-2401</idno><imprint><date when="1998">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>One important therapeutic goal during CNS injury from trauma or demyelinating diseases such as multiple sclerosis is to develop methods to promote remyelination. We tested the hypothesis that spontaneous remyelination in the toxic nonimmune model of lysolecithin-induced demyelination can be enhanced by manipulating the inflammatory response. In PBS-treated SJL/J mice, the number of remyelinating axons per square millimeter of lesion area increased significantly 3 and 5 weeks after lysolecithin injection in the spinal cord. However, methylprednisolone or a monoclonal antibody (mAb), SCH94.03, developed for its ability to promote remyelination in the Theiler’s virus murine model of demyelination, further increased the number of remyelinating axons per lesion area at 3 weeks by a factor of 2.6 and 1.9, respectively, but did not increase the ratio of myelin sheath thickness to axon diameter or the number of cells incorporating tritiated thymidine in the lesion. After 3 weeks, the number of remyelinating axons in the methylprednisolone or mAb SCH94.03 treatment groups was similar to the spontaneous remyelination in the 5 week PBS control-treated group, indicating that these treatments promoted remyelination by increasing its rate rather than its extent. To address a mechanism for promoting remyelination, through an effect on scavenger function, we assessed morphometrically the number of macrophages in lesions after methylprednisolone and mAb SCH94.03 treatment. Methylprednisolone reduced the number of macrophages, but SCH94.03 did not, although both enhanced remyelination. This study supports the hypothesis that even in toxic nonprimary immune demyelination, manipulating the inflammatory response is a benefit in myelin repair.</p></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>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Neurosci</journal-id><journal-id journal-id-type="iso-abbrev">J. Neurosci</journal-id><journal-id journal-id-type="hwp">jneuro</journal-id><journal-id journal-id-type="pmc">jneurosci</journal-id><journal-id journal-id-type="publisher-id">J. Neurosci</journal-id><journal-title-group><journal-title>The Journal of Neuroscience</journal-title></journal-title-group><issn pub-type="ppub">0270-6474</issn><issn pub-type="epub">1529-2401</issn><publisher><publisher-name>Society for Neuroscience</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">9502810</article-id><article-id pub-id-type="pmc">6793082</article-id><article-id pub-id-type="doi">10.1523/JNEUROSCI.18-07-02498.1998</article-id><article-id pub-id-type="publisher-id">1898</article-id><article-categories><subj-group subj-group-type="heading"><subject>Article</subject></subj-group></article-categories><title-group><article-title>Acceleration in the Rate of CNS Remyelination in Lysolecithin-Induced Demyelination</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Pavelko</surname><given-names>Kevin D.</given-names></name><xref ref-type="aff" rid="tO1">1</xref></contrib><contrib contrib-type="author"><name><surname>van Engelen</surname><given-names>Baziel G. M.</given-names></name><xref ref-type="aff" rid="tO1">1</xref><xref ref-type="aff" rid="tO2">2</xref></contrib><contrib contrib-type="author"><name><surname>Rodriguez</surname><given-names>Moses</given-names></name><xref ref-type="aff" rid="tO1">1</xref></contrib></contrib-group><aff id="tO1"><label><sup>1</sup></label>Departments of Neurology and Immunology, Mayo Clinic and Mayo Foundation, Rochester, Minnesota 55905, and</aff><aff id="tO2"><label><sup>2</sup></label>Institute of Neurology, University Hospital Nijmegen, 6500 HB Nijmegen, The Netherlands</aff><pub-date pub-type="ppub"><day>1</day><month>4</month><year>1998</year></pub-date><volume>18</volume><issue>7</issue><fpage>2498</fpage><lpage>2505</lpage><history><date date-type="received"><day>6</day><month>11</month><year>1997</year></date><date date-type="rev-recd"><day>13</day><month>1</month><year>1998</year></date><date date-type="accepted"><day>20</day><month>1</month><year>1998</year></date></history><permissions><copyright-statement>Copyright © 1998 Society for Neuroscience</copyright-statement><copyright-year>1998</copyright-year></permissions><abstract><p>One important therapeutic goal during CNS injury from trauma or demyelinating diseases such as multiple sclerosis is to develop methods to promote remyelination. We tested the hypothesis that spontaneous remyelination in the toxic nonimmune model of lysolecithin-induced demyelination can be enhanced by manipulating the inflammatory response. In PBS-treated SJL/J mice, the number of remyelinating axons per square millimeter of lesion area increased significantly 3 and 5 weeks after lysolecithin injection in the spinal cord. However, methylprednisolone or a monoclonal antibody (mAb), SCH94.03, developed for its ability to promote remyelination in the Theiler’s virus murine model of demyelination, further increased the number of remyelinating axons per lesion area at 3 weeks by a factor of 2.6 and 1.9, respectively, but did not increase the ratio of myelin sheath thickness to axon diameter or the number of cells incorporating tritiated thymidine in the lesion. After 3 weeks, the number of remyelinating axons in the methylprednisolone or mAb SCH94.03 treatment groups was similar to the spontaneous remyelination in the 5 week PBS control-treated group, indicating that these treatments promoted remyelination by increasing its rate rather than its extent. To address a mechanism for promoting remyelination, through an effect on scavenger function, we assessed morphometrically the number of macrophages in lesions after methylprednisolone and mAb SCH94.03 treatment. Methylprednisolone reduced the number of macrophages, but SCH94.03 did not, although both enhanced remyelination. This study supports the hypothesis that even in toxic nonprimary immune demyelination, manipulating the inflammatory response is a benefit in myelin repair.</p></abstract><kwd-group><kwd>lysolecithin</kwd><kwd>CNS</kwd><kwd>injury</kwd><kwd>demyelination</kwd><kwd>remyelination</kwd><kwd>immunoglobulin</kwd><kwd>corticosteroids</kwd><kwd>autoantibodies</kwd></kwd-group><custom-meta-group><custom-meta><meta-name>legacy-keton-price</meta-name><meta-value>5.00</meta-value></custom-meta></custom-meta-group></article-meta></front></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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