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Neuroprotective effects of mesenchymal stem cells through autophagy modulation in a parkinsonian model

 Hyun Jung Park  ;  Jin Young Shin  ;  Ha Na Kim  ;  Se Hee Oh  ;  Phil Hyu Lee 
 NEUROBIOLOGY OF AGING, Vol.35(8) : 1920-1928, 2014 
Journal Title
Issue Date
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/adverse effects ; 1-Methyl-4-phenylpyridinium/adverse effects ; Animals ; Autophagy*/drug effects ; Cell Survival*/drug effects ; Cells, Cultured ; Disease Models, Animal ; Dopaminergic Neurons/drug effects ; Dopaminergic Neurons/metabolism ; Dopaminergic Neurons/pathology* ; Humans ; Male ; Mesenchymal Stromal Cells/physiology* ; Mice, Inbred C57BL ; Neurotoxins/adverse effects ; Parkinson Disease/etiology ; Parkinson Disease/metabolism ; Parkinson Disease/pathology* ; Parkinson Disease/prevention & control* ; Protein Aggregates ; Protein Aggregation, Pathological ; alpha-Synuclein/metabolism
Autophagolysosome formation ; Autophagy ; Mesenchymal stem cells ; Parkinson's disease ; α-Synuclein
Autophagy is a major degradation pathway for abnormal aggregated proteins and organelles that cause various neurodegenerative diseases. Current evidence suggests a central role for autophagy in pathogenesis of Parkinson's disease, and that dysfunction in the autophagic system may lead to α-synuclein accumulation. In the present study, we investigated whether mesenchymal stem cells (MSCs) would enhance autophagy and thus exert a neuroprotective effect through the modulation of α-synuclein in parkinsonian models. In MPP+-treated neuronal cells, coculture with MSCs increased cellular viability, attenuated expression of α-synuclein, and enhanced the number of LC3-II-positive autophagosomes compared with cells treated with MPP+ only. In an MPTP-treated animal model of Parkinson's disease, MSC administration significantly increased final maturation of late autophagic vacuoles, fusion with lysosomes. Moreover, MSC administration significantly reduced the level of α-synuclein in dopaminergic neurons, which was elevated in MPTP-treated mice. These results suggest that MSC treatment significantly enhances autophagolysosome formation and may modulate α-synuclein expression in parkinsonian models, which may lead to increased neuronal survival in the presence of neurotoxins.
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1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > BioMedical Science Institute (의생명과학부) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Kim, Ha Na(김하나)
Park, Hyun Jung(박현정)
Shin, Jin Young(신진영)
Oh, Se Hee(오세희)
Lee, Phil Hyu(이필휴) ORCID logo https://orcid.org/0000-0001-9931-8462
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