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Neuroprotective effect of human mesenchymal stem cells in an animal model of double toxin-induced multiple system atrophy parkinsonism

DC FieldValueLanguage
dc.contributor.author김현옥-
dc.contributor.author이보라-
dc.contributor.author이필휴-
dc.date.accessioned2014-12-20T16:53:54Z-
dc.date.available2014-12-20T16:53:54Z-
dc.date.issued2011-
dc.identifier.issn0963-6897-
dc.identifier.urihttps://ir.ymlib.yonsei.ac.kr/handle/22282913/93587-
dc.description.abstractMultiple system atrophy (MSA) is an adult-onset sporadic neurodegenerative disorder of unknown etiology featuring parkinsonism, ataxia, and autonomic failure in any combination. Because disease progression in MSA is rapid and no drug treatment consistently benefits MSA patients in the long term, neuroprotective or regenerative strategies may be invaluable in the management of MSA patients. In this study, we investigated whether human mesenchymal stem cells (hMSCs) had a protective effect on MSA using an animal model of double-toxin-induced MSA parkinsonism (MSA-P). MSA-P was established with coinjections of MPTP and 3-NP; hMSCs were injected into the tail vein 1 day after the last toxin injection. Three groups of mice were compared (i.e., control, MPTP + 3-NP, and MPTP + 3-NP with hMSC treatment) through histopathological, behavioral, and Western blot analyses. In the substantia nigra (SN) and the striatum, 2.0% and 3.8% of total injected hMSCs were observed, respectively. Compared with double-toxin-treated mice, hMSC treatment in double-toxin-treated mice significantly increased survival of TH- and NeuN-immunoreactive cells in the SN and the striatum, with coincident improvement in motor behavior. Additionally, hMSC treatment significantly decreased double-toxin-induced microglial and astroglial activation in the SN and striatum. Western blot analysis showed that hMSC administration in double-toxin-treated mice increased the expression of p-Akt and Bcl-2 and decreased Bax and cytochrome c expression. This study demonstrates that hMSC treatment protected against loss of neurons in the SN and the striatum induced by double toxin exposure, which may be mediated by modulation of inflammatory and cell survival and death signaling-pathway as the hMSCs migrated from the peripheral circulation into the SN and striatum-
dc.description.statementOfResponsibilityopen-
dc.format.extent827~835-
dc.relation.isPartOfCell Transplantation-
dc.rightsCC BY-NC-ND 2.0 KR-
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/2.0/kr/-
dc.subject.MESHAnimals-
dc.subject.MESHCorpus Striatum/pathology-
dc.subject.MESHCytochromes c/metabolism-
dc.subject.MESHDisease Models, Animal-
dc.subject.MESHHumans-
dc.subject.MESHMPTP Poisoning-
dc.subject.MESHMale-
dc.subject.MESHMesenchymal Stem Cell Transplantation*-
dc.subject.MESHMice-
dc.subject.MESHMice, Inbred C57BL-
dc.subject.MESHMotor Activity/physiology-
dc.subject.MESHMultiple System Atrophy/chemically induced-
dc.subject.MESHMultiple System Atrophy/pathology-
dc.subject.MESHMultiple System Atrophy/therapy*-
dc.subject.MESHNeurotoxins/toxicity-
dc.subject.MESHNitro Compounds/toxicity-
dc.subject.MESHParkinsonian Disorders/chemically induced-
dc.subject.MESHParkinsonian Disorders/pathology-
dc.subject.MESHParkinsonian Disorders/therapy*-
dc.subject.MESHPropionates/toxicity-
dc.subject.MESHProto-Oncogene Proteins c-akt/metabolism-
dc.subject.MESHProto-Oncogene Proteins c-bcl-2/metabolism-
dc.subject.MESHSubstantia Nigra/pathology-
dc.subject.MESHbcl-2-Associated X Protein/metabolism-
dc.titleNeuroprotective effect of human mesenchymal stem cells in an animal model of double toxin-induced multiple system atrophy parkinsonism-
dc.typeArticle-
dc.contributor.collegeCollege of Medicine (의과대학)-
dc.contributor.departmentDept. of Laboratory Medicine (진단검사의학)-
dc.contributor.googleauthorPark, Hyun-Jung-
dc.contributor.googleauthorBang, Giyoon-
dc.contributor.googleauthorLee, Bo Ra-
dc.contributor.googleauthorKim, Hyun Ok-
dc.contributor.googleauthorLee, Phil Hyu-
dc.identifier.doi10.3727/096368910X540630-
dc.admin.authorfalse-
dc.admin.mappingfalse-
dc.contributor.localIdA01122-
dc.contributor.localIdA03270-
dc.contributor.localIdA02804-
dc.relation.journalcodeJ00492-
dc.identifier.pmid21054946-
dc.identifier.urlhttp://www.ingentaconnect.com/content/cog/ct/2011/00000020/00000006/art00004-
dc.subject.keywordMultiple system atrophy (MSA)-
dc.subject.keywordMesenchymal stem cells (MSCs)-
dc.subject.keywordNeuroprotection-
dc.contributor.alternativeNameKim, Hyun Ok-
dc.contributor.alternativeNameLee, Bo Ra-
dc.contributor.alternativeNameLee, Phil Hyu-
dc.contributor.affiliatedAuthorKim, Hyun Ok-
dc.contributor.affiliatedAuthorLee, Phil Hyu-
dc.contributor.affiliatedAuthorLee, Bo Ra-
dc.rights.accessRightsnot free-
dc.citation.volume20-
dc.citation.number6-
dc.citation.startPage827-
dc.citation.endPage835-
dc.identifier.bibliographicCitationCell Transplantation, Vol.20(6) : 827-835, 2011-
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Laboratory Medicine (진단검사의학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Medical Research Center (임상의학연구센터) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers

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