RETRACTED: Protective effects of transduced Tat-DJ-1 protein against oxidative stress and ischemic brain injury (Retracted article. See vol. 45, e24, 2013)
- Authors
- 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, Jinseu; Eum, Won Sik; Choi, Soo Young
- Issue Date
- 31-Oct-2012
- Publisher
- 생화학분자생물학회
- Keywords
- brain ischemia; CA1 region; hippocampal; cell survival; neurons; PARK7 protein; human; reactive oxygen species; toxicity
- Citation
- Experimental & Molecular Medicine, v.44, no.10, pp 586 - 593
- Pages
- 8
- Journal Title
- Experimental & Molecular Medicine
- Volume
- 44
- Number
- 10
- Start Page
- 586
- End Page
- 593
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/14755
- DOI
- 10.3858/emm.2012.44.10.067
- ISSN
- 1226-3613
2092-6413
- Abstract
- 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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Collections - College of Medicine > Department of Anatomy > 1. Journal Articles
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