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Induction of apoptosis signal-regulating kinase 1 and oxidative stress mediate age-dependent vulnerability to 3-nitropropionic acid in the mouse striatum

Authors
 Yangki Minn  ;  Kyoung-Joo Cho  ;  Hyun-Woo Kim  ;  Hyun-Jeong Kim  ;  Seung-Han Suk  ;  Byung I. Lee  ;  Gyung W. Kim 
Citation
 NEUROSCIENCE LETTERS, Vol.430(2) : 142-146, 2008 
Journal Title
NEUROSCIENCE LETTERS
ISSN
 0304-3940 
Issue Date
2008
MeSH
Aging/physiology* ; Animals ; Convulsants/pharmacology* ; Corpus Striatum/drug effects* ; Gene Expression Regulation/drug effects ; In Situ Nick-End Labeling/methods ; Indoles ; MAP Kinase Kinase Kinase 5/metabolism* ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Nitro Compounds/pharmacology* ; Oxidative Stress/drug effects* ; Propionates/pharmacology* ; RNA, Small Interfering/pharmacology ; Superoxide Dismutase/genetics ; Superoxide Dismutase-1
Keywords
3-Nitropropionic acid ; Oxidative stress ; Ask1 ; Aging ; Vulnerability
Abstract
The mitochondrial toxin, 3-nitropropionic acid (3-NP), produces age-dependent oxidative stress and selective striatal damage, which may simulate Huntington's disease starting in middle age. Recent reports showed that apoptosis signal-regulating kinase 1 (Ask1) activated by oxidative stress triggers a cell death signaling pathway. 3-NP was injected to the striatum in C57BL/6J mice. We have confirmed that striatal lesion volume and DNA fragmentation were age-dependent after 3-NP treatment. In the non-injured striatum of the middle-aged group, the protein levels of Ask1 and its active form, phosphorylated Ask1 (pAsk1), were significantly higher than in the young group. Ask1 increased more in the 3-NP injured striatum of the middle-aged group than in the non-injured striatum, and subsequently the activity of pAsk1 was significantly higher than in the young group. However, middle-aged SOD1Tg mice showed significant reductions of Ask1 and pAsk1 in the injured and the non-injured striatum compared to the middle-aged group. In particular, apoptosis signal transduction and cell death were significantly inhibited by the reduction of Ask1 expression using siRNA. Present results suggest that age-related upregulation of Ask1 and oxidative stress may mediate age-dependent striatal vulnerability to 3-NP.
Full Text
http://www.sciencedirect.com/science/article/pii/S0304394007011470
DOI
10.1016/j.neulet.2007.10.042
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurology (신경과학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Yonsei Biomedical Research Center (연세의생명연구원) > 1. Journal Papers
Yonsei Authors
Kim, Gyung Whan(김경환) ORCID logo https://orcid.org/0000-0001-7053-4372
Kim, Hyun Woo(김현우)
Kim, Hyun Jeong(김현정)
Lee, Byung In(이병인)
Cho, Kyuong Joo(조경주)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/106628
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