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KMID : 0624620160490070382
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BMB Reports
2016 Volume.49 No. 7 p.382 ~ p.387
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PEP-1-GSTpi protein enhanced hippocampal neuronal cell survival after oxidative damage
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Sohn Eun-Jeong
Shin Min-Jea
Kim Dae-Won
Son O-Ra
Jo Hyo-Sang
Cho Su-Bin
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 Jin-Seu
Eum Won-Sik
Choi Soo-Young
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Abstract
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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.
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KEYWORD
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Apoptotic signals, Ischemia, Oxidative stress, PEP-1-GSTpi, Protein therapy
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