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Intravenous administration of human neural stem cells induces functional recovery in Huntington's disease rat model

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dc.contributor.authorLee, Soon-Tae-
dc.contributor.authorChu, Kon-
dc.contributor.authorPark, Jung-Eun-
dc.contributor.authorLee, Kyungmi-
dc.contributor.authorKang, Lami-
dc.contributor.authorKim, Seung U-
dc.contributor.authorKim, Manho-
dc.date.accessioned2009-11-26T04:32:08Z-
dc.date.available2009-11-26T04:32:08Z-
dc.date.issued2005-05-18-
dc.identifier.citationNeurosci Res. 2005 Jul;52(3):243-9.en
dc.identifier.issn0168-0102 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=15896865-
dc.identifier.urihttps://hdl.handle.net/10371/15815-
dc.description.abstractAn animal model induced by striatal quinolinic acid (QA) injection shows ongoing striatal degeneration mimicking Huntington's disease. To study the migratory ability and the neuroprotective effect of human neural stem cells (NSCs) in this model, we transplanted NSCs (5 x 10(6)) or saline intravenously at 7 days after unilateral QA injection. NSCs-group exhibited the reduced apomorphine-induced rotation and the reduced striatal atrophy compared to the control. PCR analysis for the human-specific ERV-3 gene supported an evidence of the engraftment of human NSCs in the rat brain. X-gal+ cells were found in and around the damaged striatum and migrated NSCs differentiated into neurons and glias. This result indicates that intravenously injected human NSCs can migrate into the striatal lesion, decrease the following striatal atrophy, and induce long-term functional improvement in a glutamate toxicity-induced striatal degeneration model.en
dc.language.isoenen
dc.publisherElsevieren
dc.subjectAnimalsen
dc.subjectApomorphine/pharmacologyen
dc.subjectBehavior, Animal/drug effects/physiologyen
dc.subjectCell Count/methodsen
dc.subjectCells, Cultureden
dc.subjectCorpus Striatum/drug effects/metabolism/pathologyen
dc.subjectDNA-Binding Proteins/metabolismen
dc.subjectDisease Models, Animalen
dc.subjectDopamine and cAMP-Regulated Phosphoprotein 32en
dc.subjectDrosophila Proteins/metabolismen
dc.subjectEndogenous Retroviruses/geneticsen
dc.subjectFunctional Lateralityen
dc.subjectGalactosides/diagnostic useen
dc.subjectGlial Fibrillary Acidic Protein/metabolismen
dc.subjectHumansen
dc.subjectHuntington Disease/chemically induced/*therapyen
dc.subjectImmunohistochemistry/methodsen
dc.subjectIndoles/diagnostic useen
dc.subjectInfusions, Intravenous/*methodsen
dc.subjectMaleen
dc.subjectMotor Activity/drug effects/physiologyen
dc.subjectNerve Tissue Proteins/metabolismen
dc.subjectNeurons/*physiologyen
dc.subjectParvalbumins/metabolismen
dc.subjectPhosphoproteins/metabolismen
dc.subjectPhosphopyruvate Hydratase/metabolismen
dc.subjectQuinolinic Aciden
dc.subjectRNA, Messenger/biosynthesisen
dc.subjectRandom Allocationen
dc.subjectRatsen
dc.subjectRats, Sprague-Dawleyen
dc.subjectRecovery of Function/*physiologyen
dc.subjectReverse Transcriptase Polymerase Chain Reaction/methodsen
dc.subjectRotarod Performance Test/methodsen
dc.subjectStem Cell Transplantation/*methodsen
dc.subjectStem Cells/*physiologyen
dc.subjectTime Factorsen
dc.subjectgamma-Aminobutyric Acid/metabolismen
dc.titleIntravenous administration of human neural stem cells induces functional recovery in Huntington's disease rat modelen
dc.typeArticleen
dc.contributor.AlternativeAuthor이순태-
dc.contributor.AlternativeAuthor주건-
dc.contributor.AlternativeAuthor박정은-
dc.contributor.AlternativeAuthor이경미-
dc.contributor.AlternativeAuthor강라미-
dc.contributor.AlternativeAuthor김승유-
dc.contributor.AlternativeAuthor김만호-
dc.identifier.doi10.1016/j.neures.2005.03.016-
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