Extracts of Adipose Derived Stem Cells Slows Progression in the R6/2 Model of Huntington's Disease

被引:33
作者
Im, Wooseok [1 ]
Ban, Jaejun [1 ]
Lim, Jiyeon [1 ]
Lee, Mijung [1 ]
Lee, Soon-Tae [1 ]
Chu, Kon [1 ]
Kim, Manho [1 ]
机构
[1] Seoul Natl Univ Hosp, Biomed Res Inst, Dept Neurol, Seoul 110744, South Korea
来源
PLOS ONE | 2013年 / 8卷 / 04期
基金
新加坡国家研究基金会;
关键词
STROMAL CELLS; MOUSE MODEL; MITOCHONDRIAL DYSFUNCTION; PARACRINE MECHANISMS; MUTANT HUNTINGTIN; TRANSGENIC MOUSE; THERAPY; TISSUE; ADULT; NEURODEGENERATION;
D O I
10.1371/journal.pone.0059438
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Stem cell therapy is a promising treatment for incurable disorders including Huntington's disease (HD). Adipose-derived stem cell (ASC) is an easily available source of stem cells. Since ASCs can be differentiated into nervous stem cells, it has clinically feasible potential for neurodegenerative disease. In addition, ASCs secrete various anti-apoptotic growth factors, which improve the symptoms of disease from transplanted ASCs. Thus, cell-free extracts of ASCs (ASCs-E) could be a potential candidate for treatment of HD. Here, we investigated effects of ASCs-E on R6/2 HD mouse model and neuronal cells. In R6/2 HD model, injection of ASCs-E improved the performance in Rotarod test. ASCs-E also ameliorated striatal atrophy and mutant huntingtin aggregation in the striatum. In Western blot increased expressions of p-Akt, p-CREB and PGC1 alpha were noted by injection of ASCs-E, when comparing to the R6/2 HD model. Neuro2A neuroblastoma cells treated with ASCs-E showed increased expression of p-CREB and PGC1 alpha. In conclusion, ASCs-E delayed disease progression in animal model of HD by restoring of CREB-PGC1 alpha pathway and could be a potential resource for treatment of HD.
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页数:5
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