Dissociation of Progressive Dopaminergic Neuronal Death and Behavioral Impairments by Bax Deletion in a Mouse Model of Parkinson's Diseases
DC Field | Value | Language |
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dc.contributor.author | Kim, Tae Woo | - |
dc.contributor.author | Moon, Younghye | - |
dc.contributor.author | Kim, Kyungjin | - |
dc.contributor.author | Lee, Jeong Eun | - |
dc.contributor.author | Koh, Hyun Chul | - |
dc.contributor.author | Rhyu, Im Joo | - |
dc.contributor.author | Kim, Hyun | - |
dc.contributor.author | Sun, Woong | - |
dc.date.accessioned | 2021-09-07T07:09:28Z | - |
dc.date.available | 2021-09-07T07:09:28Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2011-10-17 | - |
dc.identifier.issn | 1932-6203 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/111363 | - |
dc.description.abstract | Parkinson's disease (PD) is a common, late-onset movement disorder with selective degeneration of dopaminergic (DA) neurons in the substantia nigra (SN). Although the neurotoxin 6-hydroxydopamine (6-OHDA) has been used to induce progressive degeneration of DA neurons in various animal models of PD, the precise molecular pathway and the impact of anti-apoptotic treatment on this neurodegeneration are less understood. Following a striatal injection of 6-OHDA, we observed atrophy and progressive death of DA neurons in wild-type mice. These degenerating DA neurons never exhibited signs of apoptosis (i.e., caspase-3 activation and cytoplasmic release of cytochrome C), but rather show nuclear translocation of apoptosis-inducing factor (AIF), a hallmark of regulated necrosis. However, mice with genetic deletion of the proapoptotic gene Bax (Bax-KO) exhibited a complete absence of 6-OHDA-induced DA neuron death and nuclear translocation of AIF, indicating that 6-OHDA-induced DA neuronal death is mediated by Bax-dependent AIF activation. On the other hand, DA neurons that survived in Bax-KO mice exhibited marked neuronal atrophy, without significant improvement of PD-related behavioral deficits. These findings suggest that anti-apoptotic therapy may not be sufficient for PD treatment, and the prevention of Bax-independent neuronal atrophy may be an important therapeutic target. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | PUBLIC LIBRARY SCIENCE | - |
dc.subject | APOPTOSIS-INDUCING FACTOR | - |
dc.subject | PROGRAMMED CELL-DEATH | - |
dc.subject | SUBSTANTIA-NIGRA | - |
dc.subject | GENE-TRANSFER | - |
dc.subject | FACTOR AIF | - |
dc.subject | RAT MODEL | - |
dc.subject | POLY(ADP-RIBOSE) POLYMERASE-1 | - |
dc.subject | NEUROMUSCULAR DEVELOPMENT | - |
dc.subject | NEUROTROPHIC FACTOR | - |
dc.subject | MOTOR DYSFUNCTION | - |
dc.title | Dissociation of Progressive Dopaminergic Neuronal Death and Behavioral Impairments by Bax Deletion in a Mouse Model of Parkinson's Diseases | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Rhyu, Im Joo | - |
dc.contributor.affiliatedAuthor | Kim, Hyun | - |
dc.contributor.affiliatedAuthor | Sun, Woong | - |
dc.identifier.doi | 10.1371/journal.pone.0025346 | - |
dc.identifier.scopusid | 2-s2.0-80054733292 | - |
dc.identifier.wosid | 000295984400010 | - |
dc.identifier.bibliographicCitation | PLOS ONE, v.6, no.10 | - |
dc.relation.isPartOf | PLOS ONE | - |
dc.citation.title | PLOS ONE | - |
dc.citation.volume | 6 | - |
dc.citation.number | 10 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Science & Technology - Other Topics | - |
dc.relation.journalWebOfScienceCategory | Multidisciplinary Sciences | - |
dc.subject.keywordPlus | APOPTOSIS-INDUCING FACTOR | - |
dc.subject.keywordPlus | PROGRAMMED CELL-DEATH | - |
dc.subject.keywordPlus | SUBSTANTIA-NIGRA | - |
dc.subject.keywordPlus | GENE-TRANSFER | - |
dc.subject.keywordPlus | FACTOR AIF | - |
dc.subject.keywordPlus | RAT MODEL | - |
dc.subject.keywordPlus | POLY(ADP-RIBOSE) POLYMERASE-1 | - |
dc.subject.keywordPlus | NEUROMUSCULAR DEVELOPMENT | - |
dc.subject.keywordPlus | NEUROTROPHIC FACTOR | - |
dc.subject.keywordPlus | MOTOR DYSFUNCTION | - |
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