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Kim, Jae-Ick
Neural Circuit and Neurodegenerative Disease Lab.
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DC Field Value Language
dc.citation.number 9 -
dc.citation.startPage e13694 -
dc.citation.title AGING CELL -
dc.citation.volume 21 - Kwon, Kujin - Cho, Hwapyeong - Lee, Soyeon - Cho, Eun Jeong - Yu, Weonjin - Kok, Catherine Yen Li - Je, Hyunsoo Shawn - Kim, Jae-Ick - Cho, Hyungjoon - Kwon, Taejoon - 2023-12-21T13:42:02Z - 2023-12-21T13:42:02Z - 2022-08-30 - 2022-09 -
dc.description.abstract Progressive iron accumulation in the substantia nigra in the aged human brain is a major risk factor for Parkinson's disease and other neurodegenerative diseases. Heavy metals, such as iron, produce reactive oxygen species and consequently oxidative stress in cells. It is unclear, however, how neurons in the substantia nigra are protected against the age-related, excessive accumulation of iron. In this study, we examined the cellular response of the substantia nigra against age-related iron accumulation in rats of different ages. Magnetic resonance imaging confirmed the presence of iron in 6-month-old rats; in 15-month-old rats, iron accumulation significantly increased, particularly in the midbrain. Transcriptome analysis of the region, in which iron deposition was observed, revealed an increase in stress response genes in older animals. To identify the genes related to the cellular response to iron, independent of neurodevelopment, we exposed the neuroblastoma cell line SH-SY5Y to a similar quantity of iron and then analyzed their transcriptomic responses. Among various stress response pathways altered by iron overloading in the rat brain and SH-SY5Y cells, the genes associated with topologically incorrect protein responses were significantly upregulated. Knockdown of HERPUD1 and CLU in this pathway increased susceptibility to iron-induced cellular stress, thus demonstrating their roles in preventing iron overload-induced toxicity. The current study details the neuronal response to excessive iron accumulation, which is associated with age-related neurodegenerative diseases. -
dc.identifier.bibliographicCitation AGING CELL, v.21, no.9, pp.e13694 -
dc.identifier.doi 10.1111/acel.13694 -
dc.identifier.issn 1474-9718 -
dc.identifier.scopusid 2-s2.0-85136477724 -
dc.identifier.uri -
dc.identifier.wosid 000842814500001 -
dc.language 영어 -
dc.publisher Blackwell Publishing Inc. -
dc.title Adaptive cellular response of the substantia nigra dopaminergic neurons upon age-dependent iron accumulation -
dc.type Article -
dc.description.isOpenAccess FALSE -
dc.relation.journalWebOfScienceCategory Cell BiologyGeriatrics & Gerontology -
dc.relation.journalResearchArea Cell BiologyGeriatrics & Gerontology -
dc.type.docType Article -
dc.description.journalRegisteredClass scie -
dc.description.journalRegisteredClass scopus -
dc.subject.keywordAuthor aging -
dc.subject.keywordAuthor iron accumulation -
dc.subject.keywordAuthor iron toxicity -
dc.subject.keywordAuthor magnetic resonance imaging -
dc.subject.keywordAuthor substantia nigra -
dc.subject.keywordAuthor transcriptome -
dc.subject.keywordPlus DYSFUNCTION -
dc.subject.keywordPlus METALS -
dc.subject.keywordPlus MYELIN -
dc.subject.keywordPlus GENOME-WIDE EXPRESSION -
dc.subject.keywordPlus PARKINSONS-DISEASE -
dc.subject.keywordPlus OXIDATIVE STRESS -
dc.subject.keywordPlus DEPOSITION -
dc.subject.keywordPlus FERRITIN -


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