Effects of low doses of Tat-PIM2 protein against hippocampal neuronal cell survival

Abstract Oxidative stress is considered a major factor in various neuronal diseases including ischemia-reperfusion injury. Proviral Integration Moloney 2 (PIM2) proteins, one of the families of PIM kinases, play crucial roles in cell survival. However, the functions of PIM2 protein against ischemia...

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Published in:Journal of the neurological sciences 2015-11, Vol.358 (1), p.226-235
Main Authors: Woo, Su Jung, Shin, Min Jea, Kim, Dae Won, Jo, Hyo Sang, In Yong, Ji, Ryu, Eun Ji, Cha, Hyun Ju, Kim, Sang Jin, Yeo, Hyeon Ji, Cho, Su Bin, Park, Jung Hwan, Lee, Chi Hern, Yeo, Eun Ji, Choi, Yeon Joo, Park, Sungyeon, Im, Seung Kwon, Kim, Duk-Soo, Kwon, Oh-Shin, Park, Jinseu, Eum, Won Sik, Choi, Soo Young
Format: Article
Language:English
Subjects:
Animals
Cell Line
Cell Survival - drug effects
Cell viability
Gene Products, tat - administration & dosage
Gerbillinae
Hippocampus - drug effects
Hippocampus - metabolism
Ischemia
MAPKs
Mice
Neurology
Neurons - drug effects
Neurons - metabolism
Oxidative stress
Oxidative Stress - drug effects
Protein therapy
Protein-Serine-Threonine Kinases - administration & dosage
Proto-Oncogene Proteins - administration & dosage
Reactive Oxygen Species - metabolism
Tat-PIM2
Transduction, Genetic
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Summary:Abstract Oxidative stress is considered a major factor in various neuronal diseases including ischemia-reperfusion injury. Proviral Integration Moloney 2 (PIM2) proteins, one of the families of PIM kinases, play crucial roles in cell survival. However, the functions of PIM2 protein against ischemia are not understood. Therefore, the protective effects of PIM2 against oxidative stress-induced hippocampal HT22 cell death and brain ischemic injury were evaluated using Tat-PIM2, a cell permeable fusion protein. Tat-PIM2 protein transduced into hippocampal HT22 cells. Low doses of transduced Tat-PIM2 protein protected against oxidative stress-induced cell death including DNA damage and markedly inhibited the activation of mitogen activated protein kinase (MAPKs), NF-κB and the expression levels of Bax protein. Furthermore, Tat-PIM2 protein transduced into the CA1 region of the hippocampus and significantly prevented neuronal cell death in an ischemic insult animal model. These results indicated that low doses of Tat-PIM2 protein protects against oxidative stress-induced neuronal cell death, suggesting low doses of Tat-PIM2 protein provides a potential therapeutic agent against oxidative stress-induced neuronal diseases including ischemia.
ISSN:0022-510X
1878-5883
DOI:10.1016/j.jns.2015.08.1549