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Overexpression of SIRT3 Suppresses Oxidative Stress-induced Neurotoxicity and Mitochondrial Dysfunction in Dopaminergic Neuronal Cells

Authors
Lee, ShinryeJeon, Yu-MiJo, MyungjinKim, Hyung-Jun
Issue Date
Oct-2021
Publisher
KOREAN SOC BRAIN & NEURAL SCIENCE, KOREAN SOC NEURODEGENERATIVE DISEASE
Keywords
Dopaminergic neuron; Mitochondrial dysfunction; Neurotoxicity; Oxidative stress; SIRT3; Astrocyte; neuron coculture
Citation
EXPERIMENTAL NEUROBIOLOGY, v.30, no.5, pp.341 - 355
Journal Title
EXPERIMENTAL NEUROBIOLOGY
Volume
30
Number
5
Start Page
341
End Page
355
URI
http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/296
DOI
10.5607/en21021
ISSN
1226-2560
Abstract
Sirtuin 3 (SIRT3), a well-known mitochondrial deacetylase, is involved in mitochondrial function and metabolism under various stress conditions. In this study, we found that the expression of SIRT3 was markedly increased by oxidative stress in dopaminergic neuronal cells. In addition, SIRT3 overexpression enhanced mitochondrial activity in differentiated SH-SY5Y cells. We also showed that SIRT3 overexpression attenuated rotenone-or H2O2-induced toxicity in differentiated SH-SY5Y cells (human dopaminergic cell line). We further found that knockdown of SIRT3 enhanced rotenone-or H2O2-induced toxicity in differentiated SH-SY5Y cells. Moreover, overexpression of SIRT3 mitigated cell death caused by LPS/IFN-gamma stimulation in astrocytes. We also found that the rotenone treatment increases the level of SIRT3 in Drosophila brain. We observed that downregu-lation of sirt2 (Drosophila homologue of SIRT3) significantly accelerated the rotenone-induced toxicity in flies. Taken together, these findings sug-gest that the overexpression of SIRT3 mitigates oxidative stress-induced cell death and mitochondrial dysfunction in dopaminergic neurons and astrocytes.
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연구본부 (치매 연구그룹)
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