| PEP-1-GSTpi protein enhanced hippocampal neuronal cell survival after oxidative damage |
| Soo Young Choi1,*, 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 |
1Hallym University, Biomedical Science and Research Institute of Bioscience and Biotechnology,
2Gangnung-Wonju National University, Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry,,
3Soonchunhyang University, Anatomy, College of Medicine,
4Biochemistry and Molecular Biology, University of Ulsan College of Medicine,
5Kyungpook National University, School of Life Sciences, College of Natural Sciences,
6Hallym University Medical Center, Neurosurgery |
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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 known to play important roles in cell survival. We investigated the effect of GSTpi against oxidative stress-induced hippocampal HT-22 cell death and in an animal model of ischemic injury using a cell-permeable PEP-1-GSTpi protein. PEP-1-GSTpi transduced into HT-22 cells and significantly protected against H2O2-treated cell death by reducing intracellular toxicity and regulation of signal pathways including MAPK, Akt, Bax, and Bcl-2. PEP-1-GSTpi transduced into hippocampus in animal brain 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 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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| Abstract, Accepted Manuscript(in press) [Submitted on March 8, 2016, Accepted on April 4, 2016] |
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