Iron accumulation promotes TACE-mediated TNF-alpha secretion and neurodegeneration in a mouse model of ALS
DC Field | Value | Language |
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dc.contributor.author | Lee, Jae Keun | - |
dc.contributor.author | Shin, Jin Hee | - |
dc.contributor.author | Gwag, Byoung Joo | - |
dc.contributor.author | Choi, Eui-Ju | - |
dc.date.accessioned | 2021-09-04T13:35:34Z | - |
dc.date.available | 2021-09-04T13:35:34Z | - |
dc.date.created | 2021-06-18 | - |
dc.date.issued | 2015-08 | - |
dc.identifier.issn | 0969-9961 | - |
dc.identifier.uri | https://scholar.korea.ac.kr/handle/2021.sw.korea/92795 | - |
dc.description.abstract | Oxidative stress contributes to degeneration of motor neurons in patients with amyotrophic lateral sclerosis (ALS) as well as transgenic mice overexpressing ALS-associated human superoxide dismutase 1 (SOD1) mutants. However, the molecular mechanism by which the ALS-linked SOD1 mutants including SOD1(G93A) induce oxidative stress remains unclear. Here, we show that iron was accumulated in ventral motor neurons from SOD1(G93A)-transgenic mice even at 4 weeks of age, subsequently inducing oxidative stress. Iron chelation with deferoxamine mesylate delayed disease onset and extended lifespan of SOD1(G93A) mice. Furthermore, SOD1(G93A)-induced iron accumulation mediated the increase in the enzymatic activity of TNF-alpha converting enzyme (TACE), leading to secretion of TNF-alpha at least in part through iron-dependent oxidative stress. Our findings suggest iron as a key determinant of early motor neuron degeneration as well as proinflammatory responses at symptomatic stage in SOD1(G93A) mice. (C) 2015 Elsevier Inc. All rights reserved. | - |
dc.language | English | - |
dc.language.iso | en | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.subject | AMYOTROPHIC-LATERAL-SCLEROSIS | - |
dc.subject | MOTOR-NEURON DEGENERATION | - |
dc.subject | NECROSIS-FACTOR-ALPHA | - |
dc.subject | SPINAL-CORD | - |
dc.subject | PROGRESSION | - |
dc.subject | DISEASE | - |
dc.subject | EXPRESSION | - |
dc.subject | SURVIVAL | - |
dc.subject | DEATH | - |
dc.title | Iron accumulation promotes TACE-mediated TNF-alpha secretion and neurodegeneration in a mouse model of ALS | - |
dc.type | Article | - |
dc.contributor.affiliatedAuthor | Choi, Eui-Ju | - |
dc.identifier.doi | 10.1016/j.nbd.2015.05.009 | - |
dc.identifier.scopusid | 2-s2.0-84952021437 | - |
dc.identifier.wosid | 000356565100006 | - |
dc.identifier.bibliographicCitation | NEUROBIOLOGY OF DISEASE, v.80, pp.63 - 69 | - |
dc.relation.isPartOf | NEUROBIOLOGY OF DISEASE | - |
dc.citation.title | NEUROBIOLOGY OF DISEASE | - |
dc.citation.volume | 80 | - |
dc.citation.startPage | 63 | - |
dc.citation.endPage | 69 | - |
dc.type.rims | ART | - |
dc.type.docType | Article | - |
dc.description.journalClass | 1 | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Neurosciences & Neurology | - |
dc.relation.journalWebOfScienceCategory | Neurosciences | - |
dc.subject.keywordPlus | AMYOTROPHIC-LATERAL-SCLEROSIS | - |
dc.subject.keywordPlus | MOTOR-NEURON DEGENERATION | - |
dc.subject.keywordPlus | NECROSIS-FACTOR-ALPHA | - |
dc.subject.keywordPlus | SPINAL-CORD | - |
dc.subject.keywordPlus | PROGRESSION | - |
dc.subject.keywordPlus | DISEASE | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | SURVIVAL | - |
dc.subject.keywordPlus | DEATH | - |
dc.subject.keywordAuthor | ALS | - |
dc.subject.keywordAuthor | Iron | - |
dc.subject.keywordAuthor | Motor neuron death | - |
dc.subject.keywordAuthor | TNF-alpha | - |
dc.subject.keywordAuthor | TNF-alpha converting enzyme (TACE) | - |
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