Overexpression of Bcl‐XL in human neural stem cells promotes graft survival and functional recovery following transplantation in spinal cord injury
Identifieur interne : 001F72 ( Main/Exploration ); précédent : 001F71; suivant : 001F73Overexpression of Bcl‐XL in human neural stem cells promotes graft survival and functional recovery following transplantation in spinal cord injury
Auteurs : Seung I. Lee [Corée du Sud] ; Byung G. Kim [Corée du Sud, Canada] ; Dong H. Hwang [Corée du Sud] ; Hyuk M. Kim [Corée du Sud] ; Seung U. Kim [Corée du Sud, Canada]Source :
- Journal of Neuroscience Research [ 0360-4012 ] ; 2009-11-01.
English descriptors
Abstract
Transplantation of neural stem cells (NSCs) has shown promise for improving functional recovery after spinal cord injury (SCI). The inhospitable milieu of injured spinal cord, however, does not support survival of grafted NSCs, reducing therapeutic efficacy of transplantation. The present study sought to examine whether overexpression of antiapoptotic gene Bcl‐XL in NSCs could promote graft survival and functional recovery following transplantation in rat contusive SCI model. A human NSC line (HB1.F3) was transduced with a retroviral vector encoding Bcl‐XL to generate Bcl‐XL‐overexpressing NSCs (HB1.F3.Bcl‐XL). Overexpression of Bcl‐XL conferred resistance to staurosporine‐mediated apoptosis. The number of HB1.F3.Bcl‐XL cells was 1.5‐fold higher at 2 weeks and 10‐fold higher at 7 weeks posttransplantation than that of HB1.F3 cells. There was no decline in the number of HB1.F3.Bcl‐XL cells between 2 and 7 weeks, indicating that Bcl‐XL overexpression completely blocked cell death occurring between these two time points. Transplantation of HB1.F3.Bcl‐XL cells improved locomotor scores and enhanced accuracy of hindlimb placement in a grid walk. Approximately 10% of surviving NSCs differentiated into oligodendrocytes. Surviving NSCs produced brain‐derived neurotrophic factor (BDNF), and the level of BDNF was significantly increased only in the HB1.F3.Bcl‐XL group. Transplantation of HB1.F3.Bcl‐XL cells reduced cavity volumes and enhanced white matter sparing. Finally, HB1.F3.Bcl‐XL grafts enhanced connectivity between the red nucleus and the spinal cord below the lesion. These results suggest that enhancing graft survival with antiapoptotic gene can potentiate therapeutic benefits of NSC‐based therapy for SCI. © 2009 Wiley‐Liss, Inc.
Url:
DOI: 10.1002/jnr.22149
Affiliations:
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Lee</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Brain Disease Research Center, Institute for Medical Sciences, Ajou University School of Medicine, Suwon</wicri:regionArea><wicri:noRegion>Suwon</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Byung G" sort="Kim, Byung G" uniqKey="Kim B" first="Byung G." last="Kim">Byung G. Kim</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Brain Disease Research Center, Institute for Medical Sciences, Ajou University School of Medicine, Suwon</wicri:regionArea><wicri:noRegion>Suwon</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Department of Neurology, Ajou University School of Medicine, Suwon</wicri:regionArea><wicri:noRegion>Suwon</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Byung G. Kim, Brain Disease Research Center, Institute for Medical Sciences, and Department of Neurology, Ajou University School of Medicine, Suwon 443‐721, KoreaSeung U. Kim, Division of Neurology, Department of Medicine, UBC Hospital, University of British Columbia, Van couver, BC V6T2B5</wicri:regionArea><wicri:noRegion>BC V6T2B5</wicri:noRegion></affiliation></author><author><name sortKey="Hwang, Dong H" sort="Hwang, Dong H" uniqKey="Hwang D" first="Dong H." last="Hwang">Dong H. Hwang</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Brain Disease Research Center, Institute for Medical Sciences, Ajou University School of Medicine, Suwon</wicri:regionArea><wicri:noRegion>Suwon</wicri:noRegion></affiliation></author><author><name sortKey="Kim, Hyuk M" sort="Kim, Hyuk M" uniqKey="Kim H" first="Hyuk M." last="Kim">Hyuk M. Kim</name><affiliation wicri:level="1"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Brain Disease Research Center, Institute for Medical Sciences, 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"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Brain Disease Research Center, Institute for Medical Sciences, Ajou University School of Medicine, Suwon</wicri:regionArea><wicri:noRegion>Suwon</wicri:noRegion></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, Department of Medicine, UBC Hospital, University of British Columbia, Vancouver, British Columbia</wicri:regionArea><wicri:noRegion>British Columbia</wicri:noRegion></affiliation><affiliation wicri:level="3"><country xml:lang="fr">Corée du Sud</country><wicri:regionArea>Medical Research Institute, Chungan University School of Medicine, Seoul</wicri:regionArea><placeName><settlement type="city">Séoul</settlement></placeName></affiliation><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Byung G. Kim, Brain Disease Research Center, Institute for Medical Sciences, and Department of Neurology, Ajou University School of Medicine, Suwon 443‐721, KoreaSeung U. Kim, Division of Neurology, Department of Medicine, UBC Hospital, University of British Columbia, Van couver, BC V6T2B5</wicri:regionArea><wicri:noRegion>BC V6T2B5</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neuroscience Research</title><title level="j" type="abbrev">J. Neurosci. 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The inhospitable milieu of injured spinal cord, however, does not support survival of grafted NSCs, reducing therapeutic efficacy of transplantation. The present study sought to examine whether overexpression of antiapoptotic gene Bcl‐XL in NSCs could promote graft survival and functional recovery following transplantation in rat contusive SCI model. A human NSC line (HB1.F3) was transduced with a retroviral vector encoding Bcl‐XL to generate Bcl‐XL‐overexpressing NSCs (HB1.F3.Bcl‐XL). Overexpression of Bcl‐XL conferred resistance to staurosporine‐mediated apoptosis. The number of HB1.F3.Bcl‐XL cells was 1.5‐fold higher at 2 weeks and 10‐fold higher at 7 weeks posttransplantation than that of HB1.F3 cells. There was no decline in the number of HB1.F3.Bcl‐XL cells between 2 and 7 weeks, indicating that Bcl‐XL overexpression completely blocked cell death occurring between these two time points. Transplantation of HB1.F3.Bcl‐XL cells improved locomotor scores and enhanced accuracy of hindlimb placement in a grid walk. Approximately 10% of surviving NSCs differentiated into oligodendrocytes. Surviving NSCs produced brain‐derived neurotrophic factor (BDNF), and the level of BDNF was significantly increased only in the HB1.F3.Bcl‐XL group. Transplantation of HB1.F3.Bcl‐XL cells reduced cavity volumes and enhanced white matter sparing. Finally, HB1.F3.Bcl‐XL grafts enhanced connectivity between the red nucleus and the spinal cord below the lesion. These results suggest that enhancing graft survival with antiapoptotic gene can potentiate therapeutic benefits of NSC‐based therapy for SCI. © 2009 Wiley‐Liss, Inc.</div></front></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, Seung I" sort="Lee, Seung I" uniqKey="Lee S" first="Seung I." last="Lee">Seung I. Lee</name></noRegion><name sortKey="Hwang, Dong H" sort="Hwang, Dong H" uniqKey="Hwang D" first="Dong H." last="Hwang">Dong H. Hwang</name><name sortKey="Kim, Byung G" sort="Kim, Byung G" uniqKey="Kim B" first="Byung G." last="Kim">Byung G. Kim</name><name sortKey="Kim, Byung G" sort="Kim, Byung G" uniqKey="Kim B" first="Byung G." last="Kim">Byung G. Kim</name><name sortKey="Kim, Hyuk M" sort="Kim, Hyuk M" uniqKey="Kim H" first="Hyuk M." last="Kim">Hyuk M. 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="Kim, Seung U" sort="Kim, Seung U" uniqKey="Kim S" first="Seung U." last="Kim">Seung U. Kim</name></country><country name="Canada"><noRegion><name sortKey="Kim, Byung G" sort="Kim, Byung G" uniqKey="Kim B" first="Byung G." last="Kim">Byung G. Kim</name></noRegion><name sortKey="Kim, Seung U" sort="Kim, Seung U" uniqKey="Kim S" first="Seung U." last="Kim">Seung U. 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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