Brain transplantation of human neural stem cells transduced with tyrosine hydroxylase and GTP cyclohydrolase 1 provides functional improvement in animal models of Parkinson disease
Identifieur interne : 000311 ( Main/Corpus ); précédent : 000310; suivant : 000312Brain transplantation of human neural stem cells transduced with tyrosine hydroxylase and GTP cyclohydrolase 1 provides functional improvement in animal models of Parkinson disease
Auteurs : Seung U. Kim ; In H. Park ; Tae H. Kim ; Kwang S. Kim ; Hyun B. Choi ; Seok H. Hong ; Jung H. Bang ; Myung A. Lee ; In S. Joo ; Chong S. Lee ; Yong S. KimSource :
- Neuropathology [ 0919-6544 ] ; 2006-04.
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Abstract
Parkinson disease is a neurodegenerative disease characterized by loss of midbrain dopaminergic neurons resulting in movement disorder. Neural stem cells (NSC) of the CNS have recently aroused a great deal of interest, not only because of their importance in basic research of neural development, but also for their therapeutic potential in neurological disorders. We have recently generated an immortalized human NSC cell line, HB1.F3, via retrovirus‐mediated v‐myc transfer. This line is capable of self‐renewal, is multipotent, and expresses cell specific markers for NSC, ATP‐binding cassettes transporter (ABCG2) and nestin. Next, we co‐transduced the F3 NSC line with genes encoding tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GTPCH1) in order to generate dopamine‐producing NSC. The F3.TH.GTPCH human NSC line expresses TH and GTPCH phenotypes as determined by RT‐PCR, western blotting and immunocytochemistry, and shows a 800 to 2000‐fold increase in production of l‐dihydroxyphenyl alanine in HPLC analysis. A marked improvement in amphetamine‐induced turning behavior was observed in parkinsonian rats implanted with F3.TH.GTPCH cells, but not in control rats receiving F3 NSC. In the animals showing functional improvement, a large number of TH‐positive F3.TH.GTPCH NSC were found at injection sites. These results indicate that human NSC, genetically transduced with TH and GTPCH1 genes, have great potential in clinical utility for cell replacement therapy in patients suffering from Parkinson disease.
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DOI: 10.1111/j.1440-1789.2006.00688.x
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Park</name><affiliation><mods:affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</mods:affiliation></affiliation></author><author><name sortKey="Kim, Tae H" sort="Kim, Tae H" uniqKey="Kim T" first="Tae H." last="Kim">Tae H. Kim</name><affiliation><mods:affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</mods:affiliation></affiliation></author><author><name sortKey="Kim, Kwang S" sort="Kim, Kwang S" uniqKey="Kim K" first="Kwang S." last="Kim">Kwang S. Kim</name><affiliation><mods:affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</mods:affiliation></affiliation></author><author><name sortKey="Choi, Hyun B" sort="Choi, Hyun B" uniqKey="Choi H" first="Hyun B." last="Choi">Hyun B. 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Kim</name><affiliation><mods:affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</mods:affiliation></affiliation></author><author><name sortKey="Choi, Hyun B" sort="Choi, Hyun B" uniqKey="Choi H" first="Hyun B." last="Choi">Hyun B. Choi</name><affiliation><mods:affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</mods:affiliation></affiliation></author><author><name sortKey="Hong, Seok H" sort="Hong, Seok H" uniqKey="Hong S" first="Seok H." last="Hong">Seok H. Hong</name><affiliation><mods:affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</mods:affiliation></affiliation></author><author><name sortKey="Bang, Jung H" sort="Bang, Jung H" uniqKey="Bang J" first="Jung H." last="Bang">Jung H. 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Lee</name><affiliation><mods:affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</mods:affiliation></affiliation></author><author><name sortKey="Kim, Yong S" sort="Kim, Yong S" uniqKey="Kim Y" first="Yong S." last="Kim">Yong S. Kim</name><affiliation><mods:affiliation>Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Neuropathology</title><idno type="ISSN">0919-6544</idno><idno type="eISSN">1440-1789</idno><imprint><publisher>Blackwell Publishing Asia</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2006-04">2006-04</date><biblScope unit="volume">26</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="129">129</biblScope><biblScope unit="page" to="140">140</biblScope></imprint><idno type="ISSN">0919-6544</idno></series><idno type="istex">F120582301D814B404BE4C86EE73788C08B6CAB0</idno><idno type="DOI">10.1111/j.1440-1789.2006.00688.x</idno><idno type="ArticleID">NEUP688</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0919-6544</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>GTP cyclohydrolase 1</term><term>HB1.F3 cell line</term><term>L‐DOPA</term><term>Parkinson disease</term><term>brain transplantation</term><term>cell therapy</term><term>neural stem cells</term><term>tyrosine hydroxylase</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Parkinson disease is a neurodegenerative disease characterized by loss of midbrain dopaminergic neurons resulting in movement disorder. Neural stem cells (NSC) of the CNS have recently aroused a great deal of interest, not only because of their importance in basic research of neural development, but also for their therapeutic potential in neurological disorders. We have recently generated an immortalized human NSC cell line, HB1.F3, via retrovirus‐mediated v‐myc transfer. This line is capable of self‐renewal, is multipotent, and expresses cell specific markers for NSC, ATP‐binding cassettes transporter (ABCG2) and nestin. Next, we co‐transduced the F3 NSC line with genes encoding tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GTPCH1) in order to generate dopamine‐producing NSC. The F3.TH.GTPCH human NSC line expresses TH and GTPCH phenotypes as determined by RT‐PCR, western blotting and immunocytochemistry, and shows a 800 to 2000‐fold increase in production of l‐dihydroxyphenyl alanine in HPLC analysis. A marked improvement in amphetamine‐induced turning behavior was observed in parkinsonian rats implanted with F3.TH.GTPCH cells, but not in control rats receiving F3 NSC. In the animals showing functional improvement, a large number of TH‐positive F3.TH.GTPCH NSC were found at injection sites. These results indicate that human NSC, genetically transduced with TH and GTPCH1 genes, have great potential in clinical utility for cell replacement therapy in patients suffering from Parkinson disease.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Seung U. Kim</name><affiliations><json:string>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</json:string><json:string>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</json:string></affiliations></json:item><json:item><name>In H. Park</name><affiliations><json:string>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</json:string></affiliations></json:item><json:item><name>Tae H. Kim</name><affiliations><json:string>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</json:string></affiliations></json:item><json:item><name>Kwang S. Kim</name><affiliations><json:string>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</json:string></affiliations></json:item><json:item><name>Hyun B. Choi</name><affiliations><json:string>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</json:string></affiliations></json:item><json:item><name>Seok H. Hong</name><affiliations><json:string>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</json:string></affiliations></json:item><json:item><name>Jung H. Bang</name><affiliations><json:string>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</json:string></affiliations></json:item><json:item><name>Myung A. Lee</name><affiliations><json:string>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</json:string></affiliations></json:item><json:item><name>In S. Joo</name><affiliations><json:string>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</json:string><json:string>Department of Neurology, Ajou University School of Medicine, Suwon, Korea and</json:string></affiliations></json:item><json:item><name>Chong S. Lee</name><affiliations><json:string>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</json:string></affiliations></json:item><json:item><name>Yong S. Kim</name><affiliations><json:string>Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>brain transplantation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cell therapy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>GTP cyclohydrolase 1</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>HB1.F3 cell line</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>L‐DOPA</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>neural stem cells</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>tyrosine hydroxylase</value></json:item></subject><articleId><json:string>NEUP688</json:string></articleId><language><json:string>eng</json:string></language><abstract>Parkinson disease is a neurodegenerative disease characterized by loss of midbrain dopaminergic neurons resulting in movement disorder. Neural stem cells (NSC) of the CNS have recently aroused a great deal of interest, not only because of their importance in basic research of neural development, but also for their therapeutic potential in neurological disorders. We have recently generated an immortalized human NSC cell line, HB1.F3, via retrovirus‐mediated v‐myc transfer. This line is capable of self‐renewal, is multipotent, and expresses cell specific markers for NSC, ATP‐binding cassettes transporter (ABCG2) and nestin. Next, we co‐transduced the F3 NSC line with genes encoding tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GTPCH1) in order to generate dopamine‐producing NSC. The F3.TH.GTPCH human NSC line expresses TH and GTPCH phenotypes as determined by RT‐PCR, western blotting and immunocytochemistry, and shows a 800 to 2000‐fold increase in production of l‐dihydroxyphenyl alanine in HPLC analysis. A marked improvement in amphetamine‐induced turning behavior was observed in parkinsonian rats implanted with F3.TH.GTPCH cells, but not in control rats receiving F3 NSC. In the animals showing functional improvement, a large number of TH‐positive F3.TH.GTPCH NSC were found at injection sites. These results indicate that human NSC, genetically transduced with TH and GTPCH1 genes, have great potential in clinical utility for cell replacement therapy in patients suffering from Parkinson disease.</abstract><qualityIndicators><score>8.104</score><pdfVersion>1.4</pdfVersion><pdfPageSize>595 x 780 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>8</keywordCount><abstractCharCount>1523</abstractCharCount><pdfWordCount>5541</pdfWordCount><pdfCharCount>35462</pdfCharCount><pdfPageCount>12</pdfPageCount><abstractWordCount>217</abstractWordCount></qualityIndicators><title>Brain transplantation of human neural stem cells transduced with tyrosine hydroxylase and GTP cyclohydrolase 1 provides functional improvement in animal models of Parkinson disease</title><genre><json:string>article</json:string></genre><host><volume>26</volume><publisherId><json:string>NEUP</json:string></publisherId><pages><total>12</total><last>140</last><first>129</first></pages><issn><json:string>0919-6544</json:string></issn><issue>2</issue><genre><json:string>Journal</json:string></genre><language><json:string>unknown</json:string></language><eissn><json:string>1440-1789</json:string></eissn><title>Neuropathology</title><doi><json:string>10.1111/(ISSN)1440-1789</json:string></doi></host><publicationDate>2006</publicationDate><copyrightDate>2006</copyrightDate><doi><json:string>10.1111/j.1440-1789.2006.00688.x</json:string></doi><id>F120582301D814B404BE4C86EE73788C08B6CAB0</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/F120582301D814B404BE4C86EE73788C08B6CAB0/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/F120582301D814B404BE4C86EE73788C08B6CAB0/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/F120582301D814B404BE4C86EE73788C08B6CAB0/fulltext/tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Brain transplantation of human neural stem cells transduced with tyrosine hydroxylase and GTP cyclohydrolase 1 provides functional improvement in animal models of Parkinson disease</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Blackwell Publishing Asia</publisher><pubPlace>Melbourne, Australia</pubPlace><availability><p>WILEY</p></availability><date>2006</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Brain transplantation of human neural stem cells transduced with tyrosine hydroxylase and GTP cyclohydrolase 1 provides functional improvement in animal models of Parkinson disease</title><author><persName><forename type="first">Seung U.</forename><surname>Kim</surname></persName><note type="correspondence"><p>Correspondence: Seung U. Kim, , PhD, Brain Disease Research Center, Ajou University School of Medicine, Suwon 442‐720, Korea. Email:</p></note><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</affiliation></author><author><persName><forename type="first">In H.</forename><surname>Park</surname></persName><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation></author><author><persName><forename type="first">Tae H.</forename><surname>Kim</surname></persName><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation></author><author><persName><forename type="first">Kwang S.</forename><surname>Kim</surname></persName><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation></author><author><persName><forename type="first">Hyun B.</forename><surname>Choi</surname></persName><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</affiliation></author><author><persName><forename type="first">Seok H.</forename><surname>Hong</surname></persName><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation></author><author><persName><forename type="first">Jung H.</forename><surname>Bang</surname></persName><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation></author><author><persName><forename type="first">Myung A.</forename><surname>Lee</surname></persName><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation></author><author><persName><forename type="first">In S.</forename><surname>Joo</surname></persName><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation><affiliation>Department of Neurology, Ajou University School of Medicine, Suwon, Korea and</affiliation></author><author><persName><forename type="first">Chong S.</forename><surname>Lee</surname></persName><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</affiliation></author><author><persName><forename type="first">Yong S.</forename><surname>Kim</surname></persName><affiliation>Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea</affiliation></author></analytic><monogr><title level="j">Neuropathology</title><idno type="pISSN">0919-6544</idno><idno type="eISSN">1440-1789</idno><idno type="DOI">10.1111/(ISSN)1440-1789</idno><imprint><publisher>Blackwell Publishing Asia</publisher><pubPlace>Melbourne, Australia</pubPlace><date type="published" when="2006-04"></date><biblScope unit="volume">26</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="129">129</biblScope><biblScope unit="page" to="140">140</biblScope></imprint></monogr><idno type="istex">F120582301D814B404BE4C86EE73788C08B6CAB0</idno><idno type="DOI">10.1111/j.1440-1789.2006.00688.x</idno><idno type="ArticleID">NEUP688</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2006</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Parkinson disease is a neurodegenerative disease characterized by loss of midbrain dopaminergic neurons resulting in movement disorder. Neural stem cells (NSC) of the CNS have recently aroused a great deal of interest, not only because of their importance in basic research of neural development, but also for their therapeutic potential in neurological disorders. We have recently generated an immortalized human NSC cell line, HB1.F3, via retrovirus‐mediated v‐myc transfer. This line is capable of self‐renewal, is multipotent, and expresses cell specific markers for NSC, ATP‐binding cassettes transporter (ABCG2) and nestin. Next, we co‐transduced the F3 NSC line with genes encoding tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GTPCH1) in order to generate dopamine‐producing NSC. The F3.TH.GTPCH human NSC line expresses TH and GTPCH phenotypes as determined by RT‐PCR, western blotting and immunocytochemistry, and shows a 800 to 2000‐fold increase in production of l‐dihydroxyphenyl alanine in HPLC analysis. A marked improvement in amphetamine‐induced turning behavior was observed in parkinsonian rats implanted with F3.TH.GTPCH cells, but not in control rats receiving F3 NSC. In the animals showing functional improvement, a large number of TH‐positive F3.TH.GTPCH NSC were found at injection sites. These results indicate that human NSC, genetically transduced with TH and GTPCH1 genes, have great potential in clinical utility for cell replacement therapy in patients suffering from Parkinson disease.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>brain transplantation</term></item><item><term>cell therapy</term></item><item><term>GTP cyclohydrolase 1</term></item><item><term>HB1.F3 cell line</term></item><item><term>L‐DOPA</term></item><item><term>neural stem cells</term></item><item><term>Parkinson disease</term></item><item><term>tyrosine hydroxylase</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2006-04">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/F120582301D814B404BE4C86EE73788C08B6CAB0/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Blackwell Publishing Asia</publisherName><publisherLoc>Melbourne, Australia</publisherLoc></publisherInfo><doi origin="wiley" registered="yes">10.1111/(ISSN)1440-1789</doi><issn type="print">0919-6544</issn><issn type="electronic">1440-1789</issn><idGroup><id type="product" value="NEUP"></id><id type="publisherDivision" value="ST"></id></idGroup><titleGroup><title type="main" sort="NEUROPATHOLOGY">Neuropathology</title></titleGroup></publicationMeta><publicationMeta level="part" position="04002"><doi origin="wiley">10.1111/neu.2006.26.issue-2</doi><numberingGroup><numbering type="journalVolume" number="26">26</numbering><numbering type="journalIssue" number="2">2</numbering></numberingGroup><coverDate startDate="2006-04">April 2006</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="4" status="forIssue"><doi origin="wiley">10.1111/j.1440-1789.2006.00688.x</doi><idGroup><id type="unit" value="NEUP688"></id></idGroup><countGroup><count type="pageTotal" number="12"></count></countGroup><titleGroup><title type="tocHeading1">ORIGINAL ARTICLES</title></titleGroup><eventGroup><event type="firstOnline" date="2006-04-10"></event><event type="publishedOnlineFinalForm" date="2006-04-10"></event><event type="xmlConverted" agent="Converter:BPG_TO_WML3G version:2.3.2 mode:FullText source:FullText result:FullText" date="2010-03-15"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-03"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst" number="129">129</numbering><numbering type="pageLast" number="140">140</numbering></numberingGroup><correspondenceTo>Seung U. Kim, <sc>md</sc>, PhD, Brain Disease Research Center, Ajou University School of Medicine, Suwon 442‐720, Korea. Email: <email>sukim@ajou.ac.kr</email></correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:NEUP.NEUP688.pdf"></link></linkGroup></publicationMeta><contentMeta><unparsedEditorialHistory>Received 24 October 2005; accepted 1 November 2005.</unparsedEditorialHistory><countGroup><count type="figureTotal" number="8"></count><count type="tableTotal" number="0"></count><count type="formulaTotal" number="0"></count><count type="referenceTotal" number="57"></count><count type="wordTotal" number="6170"></count><count type="linksPubMed" number="0"></count><count type="linksCrossRef" number="0"></count></countGroup><titleGroup><title type="main">Brain transplantation of human neural stem cells transduced with tyrosine hydroxylase and GTP cyclohydrolase 1 provides functional improvement in animal models of Parkinson disease</title><title type="shortAuthors">SU Kim <i>et al.</i></title><title type="short">Human neural stem cells for cell therapy</title></titleGroup><creators><creator creatorRole="author" xml:id="cr1" affiliationRef="#a1 #a2" corresponding="yes"><personName><givenNames>Seung U.</givenNames><familyName>Kim</familyName></personName></creator><creator creatorRole="author" xml:id="cr2" affiliationRef="#a1"><personName><givenNames>In H.</givenNames><familyName>Park</familyName></personName></creator><creator creatorRole="author" xml:id="cr3" affiliationRef="#a1"><personName><givenNames>Tae H.</givenNames><familyName>Kim</familyName></personName></creator><creator creatorRole="author" xml:id="cr4" affiliationRef="#a1"><personName><givenNames>Kwang S.</givenNames><familyName>Kim</familyName></personName></creator><creator creatorRole="author" xml:id="cr5" affiliationRef="#a2"><personName><givenNames>Hyun B.</givenNames><familyName>Choi</familyName></personName></creator><creator creatorRole="author" xml:id="cr6" affiliationRef="#a1"><personName><givenNames>Seok H.</givenNames><familyName>Hong</familyName></personName></creator><creator creatorRole="author" xml:id="cr7" affiliationRef="#a1"><personName><givenNames>Jung H.</givenNames><familyName>Bang</familyName></personName></creator><creator creatorRole="author" xml:id="cr8" affiliationRef="#a1"><personName><givenNames>Myung A.</givenNames><familyName>Lee</familyName></personName></creator><creator creatorRole="author" xml:id="cr9" affiliationRef="#a1 #a3"><personName><givenNames>In S.</givenNames><familyName>Joo</familyName></personName></creator><creator creatorRole="author" xml:id="cr10" affiliationRef="#a2"><personName><givenNames>Chong S.</givenNames><familyName>Lee</familyName></personName></creator><creator creatorRole="author" xml:id="cr11" affiliationRef="#a4"><personName><givenNames>Yong S.</givenNames><familyName>Kim</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="a1"><unparsedAffiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</unparsedAffiliation></affiliation><affiliation xml:id="a2" countryCode="CA"><unparsedAffiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</unparsedAffiliation></affiliation><affiliation xml:id="a3"><unparsedAffiliation>Department of Neurology, Ajou University School of Medicine, Suwon, Korea and</unparsedAffiliation></affiliation><affiliation xml:id="a4" countryCode="KR"><unparsedAffiliation>Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en"><keyword xml:id="k1">brain transplantation</keyword><keyword xml:id="k2">cell therapy</keyword><keyword xml:id="k3">GTP cyclohydrolase 1</keyword><keyword xml:id="k4">HB1.F3 cell line</keyword><keyword xml:id="k5">L‐DOPA</keyword><keyword xml:id="k6">neural stem cells</keyword><keyword xml:id="k7">Parkinson disease</keyword><keyword xml:id="k8">tyrosine hydroxylase</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><p>Parkinson disease is a neurodegenerative disease characterized by loss of midbrain dopaminergic neurons resulting in movement disorder. Neural stem cells (NSC) of the CNS have recently aroused a great deal of interest, not only because of their importance in basic research of neural development, but also for their therapeutic potential in neurological disorders. We have recently generated an immortalized human NSC cell line, HB1.F3, via retrovirus‐mediated v‐<i>myc</i> transfer. This line is capable of self‐renewal, is multipotent, and expresses cell specific markers for NSC, ATP‐binding cassettes transporter (ABCG2) and nestin. Next, we co‐transduced the F3 NSC line with genes encoding tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GTPCH1) in order to generate dopamine‐producing NSC. The F3.TH.GTPCH human NSC line expresses TH and GTPCH phenotypes as determined by RT‐PCR, western blotting and immunocytochemistry, and shows a 800 to 2000‐fold increase in production of <sc>l</sc>‐dihydroxyphenyl alanine in HPLC analysis. A marked improvement in amphetamine‐induced turning behavior was observed in parkinsonian rats implanted with F3.TH.GTPCH cells, but not in control rats receiving F3 NSC. In the animals showing functional improvement, a large number of TH‐positive F3.TH.GTPCH NSC were found at injection sites. These results indicate that human NSC, genetically transduced with TH and GTPCH1 genes, have great potential in clinical utility for cell replacement therapy in patients suffering from Parkinson disease.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Brain transplantation of human neural stem cells transduced with tyrosine hydroxylase and GTP cyclohydrolase 1 provides functional improvement in animal models of Parkinson disease</title></titleInfo><titleInfo type="abbreviated"><title>Human neural stem cells for cell therapy</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Brain transplantation of human neural stem cells transduced with tyrosine hydroxylase and GTP cyclohydrolase 1 provides functional improvement in animal models of Parkinson disease</title></titleInfo><name type="personal"><namePart type="given">Seung U.</namePart><namePart type="family">Kim</namePart><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</affiliation><description>Correspondence: Seung U. Kim, , PhD, Brain Disease Research Center, Ajou University School of Medicine, Suwon 442‐720, Korea. Email: </description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">In H.</namePart><namePart type="family">Park</namePart><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Tae H.</namePart><namePart type="family">Kim</namePart><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Kwang S.</namePart><namePart type="family">Kim</namePart><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Hyun B.</namePart><namePart type="family">Choi</namePart><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Seok H.</namePart><namePart type="family">Hong</namePart><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Jung H.</namePart><namePart type="family">Bang</namePart><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Myung A.</namePart><namePart type="family">Lee</namePart><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">In S.</namePart><namePart type="family">Joo</namePart><affiliation>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea;</affiliation><affiliation>Department of Neurology, Ajou University School of Medicine, Suwon, Korea and</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Chong S.</namePart><namePart type="family">Lee</namePart><affiliation>Division of Neurology, Department of Medicine, University of British Columbia, Vancouver, Canada;</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Yong S.</namePart><namePart type="family">Kim</namePart><affiliation>Department of Pharmacology, Seoul National University College of Medicine, Seoul, Korea</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article"></genre><originInfo><publisher>Blackwell Publishing Asia</publisher><place><placeTerm type="text">Melbourne, Australia</placeTerm></place><dateIssued encoding="w3cdtf">2006-04</dateIssued><edition>Received 24 October 2005; accepted 1 November 2005.</edition><copyrightDate encoding="w3cdtf">2006</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">8</extent><extent unit="references">57</extent><extent unit="words">6170</extent></physicalDescription><abstract lang="en">Parkinson disease is a neurodegenerative disease characterized by loss of midbrain dopaminergic neurons resulting in movement disorder. Neural stem cells (NSC) of the CNS have recently aroused a great deal of interest, not only because of their importance in basic research of neural development, but also for their therapeutic potential in neurological disorders. We have recently generated an immortalized human NSC cell line, HB1.F3, via retrovirus‐mediated v‐myc transfer. This line is capable of self‐renewal, is multipotent, and expresses cell specific markers for NSC, ATP‐binding cassettes transporter (ABCG2) and nestin. Next, we co‐transduced the F3 NSC line with genes encoding tyrosine hydroxylase (TH) and GTP cyclohydrolase 1 (GTPCH1) in order to generate dopamine‐producing NSC. The F3.TH.GTPCH human NSC line expresses TH and GTPCH phenotypes as determined by RT‐PCR, western blotting and immunocytochemistry, and shows a 800 to 2000‐fold increase in production of l‐dihydroxyphenyl alanine in HPLC analysis. A marked improvement in amphetamine‐induced turning behavior was observed in parkinsonian rats implanted with F3.TH.GTPCH cells, but not in control rats receiving F3 NSC. In the animals showing functional improvement, a large number of TH‐positive F3.TH.GTPCH NSC were found at injection sites. These results indicate that human NSC, genetically transduced with TH and GTPCH1 genes, have great potential in clinical utility for cell replacement therapy in patients suffering from Parkinson disease.</abstract><subject lang="en"><genre>Keywords</genre><topic>brain transplantation</topic><topic>cell therapy</topic><topic>GTP cyclohydrolase 1</topic><topic>HB1.F3 cell line</topic><topic>L‐DOPA</topic><topic>neural stem cells</topic><topic>Parkinson disease</topic><topic>tyrosine hydroxylase</topic></subject><relatedItem type="host"><titleInfo><title>Neuropathology</title></titleInfo><genre type="Journal">journal</genre><identifier type="ISSN">0919-6544</identifier><identifier type="eISSN">1440-1789</identifier><identifier type="DOI">10.1111/(ISSN)1440-1789</identifier><identifier type="PublisherID">NEUP</identifier><part><date>2006</date><detail type="volume"><caption>vol.</caption><number>26</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>129</start><end>140</end><total>12</total></extent></part></relatedItem><identifier type="istex">F120582301D814B404BE4C86EE73788C08B6CAB0</identifier><identifier type="DOI">10.1111/j.1440-1789.2006.00688.x</identifier><identifier type="ArticleID">NEUP688</identifier><recordInfo><recordContentSource>WILEY</recordContentSource><recordOrigin>Blackwell Publishing Asia</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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