Dual cell protective mechanisms activated by differing levels of oxidative stress in HT22 murine hippocampal cells
| Autor: | Ritsuko Ohtani-Kaneko, Yurina Ogura, Kazusa Ishibashi, Taku Nedachi, Masugi Nishihara, Kazunori Sato, Masaya Ishii, Yuki Yamanaka |
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| Rok vydání: | 2014 |
| Předmět: |
Cell Survival
MAP Kinase Signaling System medicine.medical_treatment Cell Hippocampus Hippocampal formation Biology Cell fate determination medicine.disease_cause Applied Microbiology and Biotechnology Biochemistry Analytical Chemistry Cell Line Mice Progranulins medicine Animals Humans Molecular Biology Granulins Neurons Growth factor Organic Chemistry Neurodegenerative Diseases General Medicine Hydrogen Peroxide Cytoprotection Cell biology Oxidative Stress medicine.anatomical_structure Cell culture Intercellular Signaling Peptides and Proteins Oxidative stress Biotechnology |
| Zdroj: | Bioscience, biotechnology, and biochemistry. 78(9) |
| ISSN: | 1347-6947 |
| Popis: | Oxidative stress is recognized as one of the pathogenic mechanisms involved in neurodegenerative disease. However, recent evidence has suggested that regulation of cellular fate in response to oxidative stress appears to be dependent on the stress levels. In this study, using HT22 cells, we attempted to understand how an alteration in the oxidative stress levels would influence neuronal cell fate. HT22 cell viability was reduced with exposure to high levels of oxidative stress, whereas, low levels of oxidative stress promoted cell survival. Erk1/2 activation induced by a low level of oxidative stress played a role in this cell protective effect. Intriguingly, subtoxic level of H2O2 induced expression of a growth factor, progranulin (PGRN), and exogenous PGRN pretreatment attenuated HT22 cell death induced by high concentrations of H2O2 in Erk1/2-dependent manner. Together, our study indicates that two different cell protection mechanisms are activated by differing levels of oxidative stress in HT22 cells. |
| Databáze: | OpenAIRE |
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