NDLI: Upregulation of Sestrin-2 Expression via P53 Protects Against 1-Methyl-4-Phenylpyridinium (MPP+) Neurotoxicity

Content Provider	Springer Nature Link
Author	Daixing, Zhou Chengye, Zhan Qiang, Zhong Shusheng, Li
Copyright Year	2013
Abstract	Sestrin-2 (SESN2) is a conserved antioxidant protein that is activated upon oxidative stress and protects cells against reactive oxygen species (ROS). However, the role of SESN2 in neurodegenerative diseases, especially in Parkinson’s disease (PD), has not yet been elucidated. In this study, we found that expression of SESN2 is elevated in the midbrain of patients with PD. Moreover, in vitro experiments display that the drug 1-methyl-4-phenylpyridinium (MPP+) induces the expression of SESN2 in SH-SY5Y cells in a time- and dose-dependent manner. Our results show that p53 is activated by MPP+. Importantly, inhibition of p53 using small RNA interferences abolishes the increased SESN2 levels induced by MPP+, suggesting that the inductive effect of MPP+ on SESN2 is mediated by p53. Furthermore, knockdown of SESN2 using small RNA interferences promotes MPP+-related neurotoxicity by attenuating oxidative stress, mitochondrial dysfunction, and apoptosis. All these data imply that the induction of SESN2 produces a protective effect in PD.
Starting Page	967
Ending Page	975
Page Count	9
File Format	PDF
ISSN	08958696
Journal	Journal of Molecular Neuroscience
Volume Number	51
Issue Number	3
e-ISSN	15591166
Language	English
Publisher	Springer US
Publisher Date	2013-08-20
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Parkinson’s disease Sestrin-2 (SESN2) p53 Oxidative stress Mitochondrial dysfunction Apoptosis Neurosciences Neurochemistry Cell Biology Proteomics Neurology
Content Type	Text
Resource Type	Article
Subject	Medicine Cellular and Molecular Neuroscience

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