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Tat-NOL3 protects against hippocampal neuronal cell death induced by oxidative stress through the regulation of apoptotic pathways.

Abstract：

:Oxidative stress-induced apoptosis is associated with neuronal cell death and ischemia. The NOL3 [nucleolar protein 3 (apoptosis repressor with CARD domain)] protein protects against oxidative stress-induced cell death. However, the protective mechanism responsible for this effect as well as the effects of NOL3 against oxidative stress in ischemia remain unclear. Thus, we examined the protective effects of NOL3 protein on hydrogen peroxide (H2O2)-induced oxidative stress and the mechanism responsible for these effects in hippocampal neuronal HT22 cells and in an animal model of forebrain ischemia using Tat-fused NOL3 protein (Tat-NOL3). Purified Tat-NOL3 protein transduced into the H2O2-exposed HT22 cells and inhibited the production of reactive oxygen species (ROS), DNA fragmentation and reduced mitochondrial membrane potential (ΔΨm). In addition, Tat-NOL3 prevented neuronal cell death through the regulation of apoptotic signaling pathways including Bax, Bcl-2, caspase-2, -3 and -8, PARP and p53. In addition, Tat-NOL3 protein transduced into the animal brains and significantly protected against neuronal cell death in the CA1 region of the hippocampus by regulating the activation of microglia and astrocytes. Taken together, these findings demonstrate that Tat-NOL3 protein protects against oxidative stress-induced neuronal cell death by regulating oxidative stress and by acting as an anti-apoptotic protein. Thus, we suggest that Tat-NOL3 represents a potential therapeutic agent for protection against ischemic brain injury.

journal_name

Int J Mol Med

journal_title

International journal of molecular medicine

authors

Sohn EJ,Shin MJ,Eum WS,Kim DW,Yong JI,Ryu EJ,Park JH,Cho SB,Cha HJ,Kim SJ,Yeo HJ,Yeo EJ,Choi YJ,Im SK,Kweon HY,Kim DS,Yu YH,Cho SW,Park M,Park J,Cho YJ,Choi SY

doi

10.3892/ijmm.2016.2596

subject

Has Abstract

pub_date

2016-07-01 00:00:00

pages

225-35

issue

1

eissn

1107-3756

issn

1791-244X

journal_volume

38

pub_type

杂志文章

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