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KMID : 0620920120440100586
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Experimental & Molecular Medicine
2012 Volume.44 No. 10 p.586 ~ p.593
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Protective effects of transduced Tat-DJ-1 protein against oxidative stress and ischemic brain injury
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Jeong Hoon-Jae
Kim Dae-Won
Kim Mi-Jin
Woo Su-Jung
Kim Hye-Ri
Kim So-Mi
Jo Hyo-Sang
Hwang Hyun-Sook
Kim Duk-Soo
Cho Sung-Woo
Won Moo-Ho
Han Kyu-Hyung
Park Jin-Seu
Eum Won-Sik
Choi Soo-Young
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Abstract
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Reactive oxygen species (ROS) contribute to the development of a number of neuronal diseases including ischemia. DJ-1, also known to PARK7, plays an important role in transcriptional regulation, acting as molecular chaperone and antioxidant. In the present study, we investigated whether DJ-1 protein shows a protective effect against oxidative stress-induced neuronal cell death in vitro and in ischemic animal models in vivo. To explore DJ-1 protein's potential role in protecting against ischemic cell death, we constructed cell permeable Tat-DJ-1 fusion proteins. Tat-DJ-1 protein efficiently transduced into neuronal cells in a dose- and time-dependent manner. Transduced Tat-DJ-1 protein increased cell survival against hydrogen peroxide (H2O2) toxicity and also reduced intracellular ROS. In addition, Tat-DJ-1 protein inhibited DNA fragmentation induced by H2O2. Furthermore, in animal models, immunohistochemical analysis revealed that Tat-DJ-1 protein prevented neuronal cell death induced by transient forebrain ischemia in the CA1 region of the hippocampus. These results demonstrate that transduced Tat-DJ-1 protein protects against cell death in vitro and in vivo, suggesting that the transduction of Tat-DJ-1 may be useful as a therapeutic agent for ischemic injuries related to oxidative stress.
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KEYWORD
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brain ischemia, CA1 region, hippocampal, cell survival, neurons, PARK7 protein, human, reactive oxygen species, toxicity
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