Induction of GAP-43 modulates neuroplasticity in PBSC (CD34+) implanted-Parkinson's model

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 periphera...

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Published in:Journal of neuroscience research 2009-07, Vol.87 (9), p.2020-2033
Main Authors: Shyu, Woei-Cherng, Li, Kuo-Wei, Peng, Hsiao-Fen, Lin, Shinn-Zong, Liu, Ren-Shyan, Wang, Hsiao-Jung, Su, Ching-Yuan, Lee, Yih-Jing, Li, Hung
Format: Article
Language:English
Subjects:
1H-MRS
6-OHDA lesioning
Animals
Antigens, CD34 - metabolism
Biomarkers - metabolism
Brain-Derived Neurotrophic Factor - metabolism
CD34
Cell Survival - physiology
Corpus Striatum - cytology
Corpus Striatum - metabolism
Corpus Striatum - surgery
Denervation
Disease Models, Animal
Dopamine - metabolism
Excitatory Amino Acid Antagonists - pharmacology
FDG-PET
Fluorodeoxyglucose F18
GAP-43 Protein - metabolism
Glucose - metabolism
growth-associated protein 43 (GAP-43)
Male
Neuronal Plasticity - physiology
Oxidopamine
Parkinson's disease
Parkinsonian Disorders - metabolism
Parkinsonian Disorders - physiopathology
Parkinsonian Disorders - surgery
Peripheral Blood Stem Cell Transplantation - methods
peripheral blood stem cells
Positron-Emission Tomography
Rats
Rats, Sprague-Dawley
Recovery of Function - physiology
Stem Cells - cytology
Stem Cells - immunology
Stem Cells - metabolism
Substantia Nigra - cytology
Substantia Nigra - metabolism
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Summary: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. © 2009 Wiley‐Liss, Inc.
ISSN:0360-4012
1097-4547
1097-4547
DOI:10.1002/jnr.22027