BMB Rep. 2016; 49(7): 382-387  
PEP-1-GSTpi protein enhanced hippocampal neuronal cell survival after oxidative damage
Eun Jeong Sohn1,#, Min Jea Shin1,#, Dae Won Kim2,#, Ora Son1, Hyo Sang Jo1, Su Bin Cho1, Jung Hwan Park1, Chi Hern Lee1, Eun Ji Yeo1, Yeon Joo Choi1, Yeon Hee Yu3, Duk-Soo Kim3, Sung-Woo Cho4, Oh Shin Kwon5, Yong-Jun Cho6, Jinseu Park1, Won Sik Eum1,* & Soo Young Choi1,*
1Department of Biomedical Science and Research Institute of Bioscience and Biotechnology, Hallym University, Chunchon 24252, 2Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangnung-Wonju National University, Gangneung 25457, 3Department of Anatomy, College of Medicine, Soonchunhyang University, Cheonan 31538, 4Department of Biochemistry and Molecular Biology, University of Ulsan College of Medicine, Seoul 05505, 5School of Life Sciences, College of Natural Sciences, Kyungpook National University, Daegu 41566, 6Department of Neurosurgery, Hallym University Medical Center, Chuncheon 24253, Korea
Correspondence to: Soo Young Choi, Tel: +82-33-248-2112; Fax: +82-33-241-1463; E-mail:, Won Sik Eum, Tel: +82-33-248-2112; Fax: +82-33-241-1463; E-mail: #These authors contributed equally to this work.
Received: March 8, 2016; Revised: March 28, 2016; Accepted: April 4, 2016; Published online: July 31, 2016.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

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 stressinduced 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.
Keywords: Apoptotic signals, Ischemia, Oxidative stress, PEP-1-GSTpi, Protein therapy

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