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Axotomy-induced dopaminergic neurodegeneration is accompanied with c-Jun phosphorylation and activation transcription factor 3 expression

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Author(s)
Dae Y. SongYoung C. YangDong H. ShinShuei SugamaYoon S. KimBong H. LeeTong H. JohByung P. Cho
Keimyung Author(s)
Shin, Dong Hoon
Department
Dept. of Preventive Medicine (예방의학)
Brain Research Institute (뇌연구소)
Journal Title
Experimental Neurology
Issued Date
2008
Volume
209
Issue
1
Abstract
Accumulating evidence has shown that both phosphorylated c-Jun (pc-Jun) and activating transcription factor 3 (ATF3) were upregulated in a
variety of tissue injuries and proposed to play an important role in cell death/survival. To elucidate the significance and functional role of these
immediate-early genes during neuronal damage in the central nervous system, we examined temporal and spatial profiles of pc-Jun and ATF3 in
dopaminergic neurons of the substantia nigra (SN) following transection of the medial forebrain bundle (MFB) in adult rats. Morphological
characteristics of pc-Jun-positive dopaminergic neurons as well as microglial reaction in response to the axotomy-induced neurodegeneration were
also investigated. Following MFB transection, both c-Jun phosphorylation and ATF3 were found in the nuclei of tyrosine hydroxylaseimmunoreactive
(TH-ir) neurons of the ipsilateral SN, but not in those of the contralateral SN. In the ipsilateral SN, the number of pc-Jun- and
ATF3-positive nuclei was increased by 5–7 days post-lesion, and then progressively decreased probably due to the loss of neurons. Retrograde
tracing with FluoroGold (FG) in hemi-axotomized rat brain demonstrated that none of the intact, unaxotomized (FG-ir) neurons was pc-Junpositive,
indicating phosphorylation of c-Jun occurs only in axotomized neurons. Concomitant co-localization of pc-Jun and ATF3 in the same
TH-ir neuron was also demonstrated by triple immunofluorescence labeling. Many TH-ir neurons that underwent various steps of consecutive
neurodegenerative changes retained pc-Jun in the condensed or fragmented nuclei. Moreover, numerous activated microglia, identified by both
phagocytic (ED1) and MHC II (OX6) markers, closely apposed to these neurons throughout the entire neurodegenerative process, suggesting that
they are actively phagocytosing dying neurons. Taken together, these results support the idea that pc-Jun and its putative dimeric partner ATF3
may be closely participating in axotomy-induced neurodegeneration.
© 2007 Elsevier Inc. All rights reserved.
Keimyung Author(s)(Kor)
신동훈
Publisher
School of Medicine
Citation
Dae Y. Song et al. (2008). Axotomy-induced dopaminergic neurodegeneration is accompanied with
c-Jun phosphorylation and activation transcription factor 3 expression. Experimental Neurology, 209(1), 268–278. doi: 10.1016/j.expneurol.2007.09.033
Type
Article
ISSN
0014-4886
Source
https://www.sciencedirect.com/science/article/pii/S0014488607003731?via%3Dihub
DOI
10.1016/j.expneurol.2007.09.033
URI
https://kumel.medlib.dsmc.or.kr/handle/2015.oak/35733
Appears in Collections:
3. Research Institutues (연구소) > Brain Research Institute (뇌연구소)
1. School of Medicine (의과대학) > Dept. of Preventive Medicine (예방의학)
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