PEP-1-GSTpi protein enhanced hippocampal neuronal cell survival after oxidative damage
- Authors
- Sohn, Eun Jeong; Shin, Min Jea; Kim, Dae Won; Son, Ora; Jo, Hyo Sang; Bin Cho, Su; Park, Jung Hwan; Lee, Chi Hern; Yeo, Eun Ji; Choi, Yeon Joo; Yu, Yeon Hee; Kim, Duk-Soo; Cho, Sung-Woo; Kwon, Oh Shin; Cho, Yong-Jun; Park, Jinseu; Eum, Won Sik; Choi, Soo Young
- Issue Date
- 31-Jul-2016
- Publisher
- 생화학분자생물학회
- Keywords
- Apoptotic signals; Ischemia; Oxidative stress; PEP-1-GSTpi; Protein therapy
- Citation
- BMB Reports, v.49, no.7, pp 382 - 387
- Pages
- 6
- Journal Title
- BMB Reports
- Volume
- 49
- Number
- 7
- Start Page
- 382
- End Page
- 387
- URI
- https://scholarworks.bwise.kr/sch/handle/2021.sw.sch/8931
- DOI
- 10.5483/BMBRep.2016.49.7.048
- ISSN
- 1976-6696
1976-670X
- Abstract
- Reactive oxygen species generated under oxidative stress are involved in neuronal diseases, including ischemia. Glutathione S-transferase pi (GSTpi) is a member of the GST family and is known to play important roles in cell survival. We investigated the effect of GSTpi against oxidative stress-induced hippocampal HT-22 cell death, and its effects in an animal model of ischemic injury, using a cell-permeable PEP-1-GSTpi protein. PEP-1-GSTpi was transduced into HT-22 cells and significantly protected against H2O2-treated cell death by reducing the intracellular toxicity and regulating the signal pathways, including MAPK, Akt, Bax, and Bcl-2. PEP-1-GSTpi transduced into the hippocampus in animal brains, and markedly protected against neuronal cell death in an ischemic injury animal model. These results indicate that PEP-1-GSTpi acts as a regulator or an antioxidant to protect against oxidative stress-induced cell death. Our study suggests that PEP-1-GSTpi may have potential as a therapeutic agent for the treatment of ischemia and a variety of oxidative stress-related neuronal diseases.
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