Induction of GAP-43 Modulates Neuroplasticity in PBSC (CD34+) Implanted-Parkinson’s Model

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Title:	Induction of GAP-43 Modulates Neuroplasticity in PBSC (CD34+) Implanted-Parkinson’s Model
Authors:	徐偉成(Woei-Cherng Shyu);(Kuo-wei Li);(Hsiao Fen Peng);林欣榮(Shinn-Zong Lin);(Ren Shyan Liu);(Hsiao Jung Wang);(Ching Yuan Su);(Yih Jing Lee);李鴻(HUNG LI)*
Contributors:	醫學院免疫學研究所;中國附醫神經部
Keywords:	6-OHDA lesioning;Parkinson's disease;peripheral blood stem cells;CD34;growth-associated protein 43 (GAP-43);1H-MRS;FDG-PET
Date:	2009-02
Issue Date:	2010-09-27 15:42:50 (UTC+8)
Abstract:	As a result of the progressive decrease in efficacy of drugs used to treat Parkinson's disease (PD) and the rapid development of motor complications, effective alternative treatments for PD are required. In a 6-hydroxydopamine (6-OHDA)-induced Parkinson's rat model, intracerebral peripheral blood stem cell (CD34+) (PBSC) transplantation significantly protected dopaminergic neurons from 6-OHDA-induced neurotoxicity, enhanced neural repair of tyrosine hydroxylase neurons through up-regulation of Bcl-2, facilitated stem cell plasticity, and attenuated activation of microglia, in comparison with vehicle-control rats. The 6-OHDA-lesioned hemi-Parkinsonian rats receiving intrastriatal transplantation of PBSCs also showed: 1) enhanced glucose metabolism in the lesioned striatum and thalamus, demonstrated by [18F]fluoro-2-deoxyglucose positron emission tomography (FDG-PET), 2) improved neurochemical activity as shown by proton magnetic resonance spectroscopy (1H-MRS), and 3) significantly reduced rotational behavior in comparison with control lesioned rats. These observations might be explained by an up-regulation of growth-associated protein 43 (GAP-43) expression because improvements in neurological dysfunction were blocked by injection of MK-801 in the PBSC-treated group. In addition, a significant increase in neurotrophic factor expression was found in the ipsilateral hemisphere of the PBSC-treated group. In summary, this protocol may be a useful strategy for the treatment of clinical PD.
Relation:	JOURNAL OF NEUROSCIENCE RESEARCH (87):2020-2033
Appears in Collections:	[Graduate Institute of Immunology] Journal articles

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