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Proactive transplantation of human neural stem cells prevents degeneration of striatal neurons in a rat model of Huntington disease.

Authors
Ryu, JK; Kim, J; Cho, SJ; Hatori, K; Nagai, A; Choi, HB; Lee, MC; McLarnon, JG; Kim, SU
Citation
Neurobiology of disease, 16(1):68-77, 2004
Journal Title
Neurobiology of disease
ISSN
0969-99611095-953X
Abstract
We have investigated the effectiveness of transplantation of human neural stem cells into adult rat striatum prior to induction of striatal damage with the mitochondrial toxin 3-nitropropionic acid (3-NP). Systemic 3-NP administration caused widespread neuropathological deficits similar to ones found in Huntington disease (HD) including impairment in motor function (rotarod balance test) and extensive degeneration of neuron-specific nuclear antigen (NeuN)(+) neurons, calbindin(+) neurons and glutamic acid decarboxylase (GAD)(+) striatal neurons. Animals receiving intrastriatal implantation of human neural stem cells (hNSCs) 1 week before 3-NP treatments exhibited significantly improved motor performance and reduced damage to striatal neurons compared with control sham injections. In contrast, transplantation of hNSCs at 12 h after the initial 3-NP administration did not lead to any improvement in motor performance or protect striatal neurons from the 3-NP-induced toxicity. These results indicate that the presence of grafted hNSCs before 3-NP treatment is required for host striatal neuronal protection and enhanced motor function. Immunoreactivity of brain-derived neurotrophic factor (BDNF) was found in vitro in cultured hNSCs and in vivo in grafted NSCs with expression and secretion of BDNF demonstrated by RT-PCR, immunocytochemistry, dot-blot, and ELISA analyses. Thus, protective effects of proactive transplantation of hNSCs may be due, in part, to effects mediated by BDNF. The findings in this work have particular relevance to a rat model of HD in that proactive transplanted hNSCs protect host striatal neurons against neuronal injury and improve motor impairment induced by 3-NP toxicity.
MeSH terms
AnimalsCell Line, TransformedCorpus Striatum/pathology/*transplantation*Disease Models, AnimalHumansHuntington Disease/pathology/*surgeryMaleNerve Degeneration/pathology/*prevention & control/surgeryNeurons/*transplantationRatsRats, Inbred LewStem Cell Transplantation/*methodsStem Cells/*physiologyTelencephalon/transplantation
DOI
10.1016/j.nbd.2004.01.016
PMID
15207263
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Neurology
AJOU Authors
김, 승업
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