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Neuroprotective effect of neural stem cell-conditioned media in in vitro model of Huntington's disease

Cited 12 time in Web of Science Cited 12 time in Scopus
Authors
Lim, Heon-Chang; Lee, Soon-Tae; Chu, Kon; Joo, Kyung Min; Kang, Lami; Im, Woo-Seok; Park, Joung-Eun; Kim, Seung U; Kim, Manho; Cha, Choong-Ik
Issue Date
2008-03-18
Publisher
Elsevier
Citation
Neurosci Lett. 435 (2008) 175-180
Keywords
Apoptosis/drug effectsCells, CulturedCulture Media, Conditioned/*pharmacologyDose-Response Relationship, DrugFetusFlow Cytometry/methodsHumansNerve Tissue Proteins/genetics/metabolismNeurons/chemistry/*drug effectsNeuroprotective Agents/*pharmacologyNuclear Proteins/geneticsStem Cells/*chemistryTelencephalon/cytologyTransfection/methodsTrinucleotide Repeat Expansion/*genetics
Abstract
Although neural stem cell (NSC) transplantation has been investigated as a promising tool for reconstituting damaged brains, recent evidences suggest that NSCs may rescue the brain via paracrine effects rather than by direct cell replacements. In this study, we attempted to determine the neuroprotective effect of NSC-conditioned media (NSC-CM) in in vitro model of Huntington's disease. Cerebral hybrid neurons (A1) were transfected with either wild-type huntingtin (18 CAG repeats) or mutant huntingtin (100 CAG repeats). At 24h after the transfection, immunocytochemical patterns of the huntingtin aggregations, as well as the level of N-terminal proteolytic cleavages of huntingtin were analyzed. Neuronal apoptosis was evaluated with flowcytometry after Annexin-V and propidium iodide (PI) staining. Cerebral hybrid neurons transfected with mutant huntingtin showed five aggregates patterns, including diffuse cytoplasmic, dispered vacuoles, perinuclear vacuoles, nuclear inclusions (NI), and cytoplasmic inclusions (CI). NSC-CM reduced the levels of nuclear and cytoplasmic inclusions. The transfection with mutant huntingtin increased the level of N-terminal cleavages, which was reduced by the NSC-CM treatment. In addition, NSC-CM reduced the Annexin-V(+)PI(+) and Annexin-V(+)PI(-) neurons which were induced by the mutant huntingtin transfection. In summary, NSC-CM was neuroprotective in in vitro model of Huntington's disease with modulating mutant huntingtin-induced cytotoxicity.
ISSN
0304-3940 (Print)
Language
English
URI
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18343580

http://www.sciencedirect.com/science?_ob=MImg&_imagekey=B6T0G-4S1C8H0-3-5&_cdi=4862&_user=168665&_orig=search&_coverDate=04%2F25%2F2008&_sk=995649996&view=c&wchp=dGLbVtb-zSkzk&md5=446f82982b28642d534d950fca8e1ac0&ie=/sdarticle.pdf

http://hdl.handle.net/10371/68452
DOI
https://doi.org/10.1016/j.neulet.2008.02.035
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College of Medicine/School of Medicine (의과대학/대학원)Dept. of Neurology (신경과학교실)Journal Papers (저널논문_신경과학교실)
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