Dual cell protective mechanisms activated by differing levels of oxidative stress in HT22 murine hippocampal cells

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 attempte...

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Bibliographic Details
Published in:Bioscience, biotechnology, and biochemistry biotechnology, and biochemistry, 2014-09, Vol.78 (9), p.1495-1503
Main Authors: Sato, Kazunori, Yamanaka, Yuki, Ishii, Masaya, Ishibashi, Kazusa, Ogura, Yurina, Ohtani-Kaneko, Ritsuko, Nishihara, Masugi, Nedachi, Taku
Format: Article
Language:English
Subjects:
Animals
Cell Line
Cell Survival - drug effects
Cytoprotection - drug effects
Erk1/2
Hippocampus - drug effects
Hippocampus - metabolism
Hippocampus - pathology
HT22 cells
Humans
Hydrogen Peroxide - toxicity
Intercellular Signaling Peptides and Proteins - biosynthesis
MAP Kinase Signaling System - drug effects
Mice
Neurodegenerative Diseases - etiology
Neurodegenerative Diseases - metabolism
Neurodegenerative Diseases - pathology
Neurons - drug effects
Neurons - pathology
Oxidative Stress
progranulin
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Summary: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 H 2 O 2 induced expression of a growth factor, progranulin (PGRN), and exogenous PGRN pretreatment attenuated HT22 cell death induced by high concentrations of H 2 O 2 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. Two distinct cell-protective mechanisms are activated in response to different levels of oxidative stress in HT22 cells.
ISSN:0916-8451
1347-6947
DOI:10.1080/09168451.2014.936343