Human Neural Stem Cells Over-Expressing VEGF Provide Neuroprotection, Angiogenesis and Functional Recovery in Mouse Stroke Model
Identifieur interne : 002469 ( Main/Exploration ); précédent : 002468; suivant : 002470Human Neural Stem Cells Over-Expressing VEGF Provide Neuroprotection, Angiogenesis and Functional Recovery in Mouse Stroke Model
Auteurs : Hong J. Lee [Corée du Sud, Canada] ; Kwang S. Kim [Corée du Sud, Canada] ; In H. Park [Corée du Sud] ; Seung U. Kim [Corée du Sud, Canada]Source :
- PLoS ONE [ 1932-6203 ] ; 2007.
Abstract
Intracerebral hemorrhage (ICH) is a lethal stroke type. As mortality approaches 50%, and current medical therapy against ICH shows only limited effectiveness, an alternative approach is required, such as stem cell-based cell therapy. Previously we have shown that intravenously transplanted human neural stem cells (NSCs) selectively migrate to the brain and induce behavioral recovery in rat ICH model, and that combined administration of NSCs and vascular endothelial growth factor (VEGF) results in improved structural and functional outcome from cerebral ischemia.
We postulated that human NSCs overexpressing VEGF transplanted into cerebral cortex overlying ICH lesion could provide improved survival of grafted NSCs, increased angiogenesis and behavioral recovery in mouse ICH model. ICH was induced in adult mice by unilateral injection of bacterial collagenase into striatum. HB1.F3.VEGF human NSC line produced an amount of VEGF four times higher than parental F3 cell line in vitro, and induced behavioral improvement and 2–3 fold increase in cell survival at two weeks and eight weeks post-transplantation.
Brain transplantation of F3 human NSCs over-expressing VEGF near ICH lesion sites provided differentiation and survival of grafted human NSCs and renewed angiogenesis of host brain and functional recovery of ICH animals. These results suggest a possible application of the human neural stem cell line, which is genetically modified to over-express VEGF, as a therapeutic agent for ICH-stroke.
Url:
DOI: 10.1371/journal.pone.0000156
PubMed: 17225860
PubMed Central: 1764718
Affiliations:
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Lee</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</addr-line></nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Brain Disease Research Center, Ajou University School of Medicine, Suwon</wicri:regionArea><wicri:noRegion>Suwon</wicri:noRegion></affiliation><affiliation wicri:level="3"><nlm:aff id="aff2"><addr-line>College of Bioscience and Biotechnology, Korea University, Seoul, Korea</addr-line></nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Bioscience and Biotechnology, Korea University, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement></placeName></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><addr-line>Division of Neurology, Department of Medicine, University of British Columbia Hospital, University of British Columbia, Vancouver, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Department of Medicine, University of British Columbia Hospital, University of British Columbia, Vancouver</wicri:regionArea><wicri:noRegion>Vancouver</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Kwang S" sort="Kim, Kwang S" uniqKey="Kim K" first="Kwang S." last="Kim">Kwang S. 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Lee</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</addr-line></nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Brain Disease Research Center, Ajou University School of Medicine, Suwon</wicri:regionArea><wicri:noRegion>Suwon</wicri:noRegion></affiliation><affiliation wicri:level="3"><nlm:aff id="aff2"><addr-line>College of Bioscience and Biotechnology, Korea University, Seoul, Korea</addr-line></nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>College of Bioscience and Biotechnology, Korea University, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement></placeName></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><addr-line>Division of Neurology, Department of Medicine, University of British Columbia Hospital, University of British Columbia, Vancouver, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Department of Medicine, University of British Columbia Hospital, University of British Columbia, Vancouver</wicri:regionArea><wicri:noRegion>Vancouver</wicri:noRegion></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 wicri:level="1"><nlm:aff id="aff1"><addr-line>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</addr-line></nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Brain Disease Research Center, Ajou University School of Medicine, Suwon</wicri:regionArea><wicri:noRegion>Suwon</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><addr-line>Division of Neurology, Department of Medicine, University of British Columbia Hospital, University of British Columbia, Vancouver, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Department of Medicine, University of British Columbia Hospital, University of British Columbia, Vancouver</wicri:regionArea><wicri:noRegion>Vancouver</wicri:noRegion></affiliation></author><author><name sortKey="Park, In H" sort="Park, In H" uniqKey="Park I" first="In H." last="Park">In H. Park</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</addr-line></nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Brain Disease Research Center, Ajou University School of Medicine, Suwon</wicri:regionArea><wicri:noRegion>Suwon</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Seung U" sort="Kim, Seung U" uniqKey="Kim S" first="Seung U." last="Kim">Seung U. Kim</name><affiliation wicri:level="1"><nlm:aff id="aff1"><addr-line>Brain Disease Research Center, Ajou University School of Medicine, Suwon, Korea</addr-line></nlm:aff><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Brain Disease Research Center, Ajou University School of Medicine, Suwon</wicri:regionArea><wicri:noRegion>Suwon</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="aff3"><addr-line>Division of Neurology, Department of Medicine, University of British Columbia Hospital, University of British Columbia, Vancouver, Canada</addr-line></nlm:aff><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Department of Medicine, University of British Columbia Hospital, University of British Columbia, Vancouver</wicri:regionArea><wicri:noRegion>Vancouver</wicri:noRegion></affiliation></author></analytic><series><title level="j">PLoS ONE</title><idno type="eISSN">1932-6203</idno><imprint><date when="2007">2007</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Background</title><p>Intracerebral hemorrhage (ICH) is a lethal stroke type. As mortality approaches 50%, and current medical therapy against ICH shows only limited effectiveness, an alternative approach is required, such as stem cell-based cell therapy. Previously we have shown that intravenously transplanted human neural stem cells (NSCs) selectively migrate to the brain and induce behavioral recovery in rat ICH model, and that combined administration of NSCs and vascular endothelial growth factor (VEGF) results in improved structural and functional outcome from cerebral ischemia.</p></sec><sec><title>Methods and Findings</title><p>We postulated that human NSCs overexpressing VEGF transplanted into cerebral cortex overlying ICH lesion could provide improved survival of grafted NSCs, increased angiogenesis and behavioral recovery in mouse ICH model. ICH was induced in adult mice by unilateral injection of bacterial collagenase into striatum. HB1.F3.VEGF human NSC line produced an amount of VEGF four times higher than parental F3 cell line in vitro, and induced behavioral improvement and 2–3 fold increase in cell survival at two weeks and eight weeks post-transplantation.</p></sec><sec><title>Conclusions</title><p>Brain transplantation of F3 human NSCs over-expressing VEGF near ICH lesion sites provided differentiation and survival of grafted human NSCs and renewed angiogenesis of host brain and functional recovery of ICH animals. These results suggest a possible application of the human neural stem cell line, which is genetically modified to over-express VEGF, as a therapeutic agent for ICH-stroke.</p></sec></div></front><back><div1 type="bibliography"><listBibl><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct><biblStruct></biblStruct></listBibl></div1></back></TEI><affiliations><list><country><li>Canada</li><li>Corée du Sud</li></country><settlement><li>Séoul</li></settlement></list><tree><country name="Corée du Sud"><noRegion><name sortKey="Lee, Hong J" sort="Lee, Hong J" uniqKey="Lee H" first="Hong J." last="Lee">Hong J. Lee</name></noRegion><name sortKey="Kim, Kwang S" sort="Kim, Kwang S" uniqKey="Kim K" first="Kwang S." last="Kim">Kwang S. Kim</name><name sortKey="Kim, Seung U" sort="Kim, Seung U" uniqKey="Kim S" first="Seung U." last="Kim">Seung U. Kim</name><name sortKey="Lee, Hong J" sort="Lee, Hong J" uniqKey="Lee H" first="Hong J." last="Lee">Hong J. Lee</name><name sortKey="Park, In H" sort="Park, In H" uniqKey="Park I" first="In H." last="Park">In H. Park</name></country><country name="Canada"><noRegion><name sortKey="Lee, Hong J" sort="Lee, Hong J" uniqKey="Lee H" first="Hong J." last="Lee">Hong J. Lee</name></noRegion><name sortKey="Kim, Kwang S" sort="Kim, Kwang S" uniqKey="Kim K" first="Kwang S." last="Kim">Kwang S. Kim</name><name sortKey="Kim, Seung U" sort="Kim, Seung U" uniqKey="Kim S" first="Seung U." last="Kim">Seung U. Kim</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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