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Role of MAPK/ERK1/2 in the glucose deprivation-induced death in immunostimulated astroglia

Title
Role of MAPK/ERK1/2 in the glucose deprivation-induced death in immunostimulated astroglia
Authors
Yoo B.K.Choi J.W.Han B.H.Kim W.-K.Kim H.-C.Ko K.H.
Ewha Authors
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Issue Date
2005
Journal Title
Neuroscience Letters
ISSN
0304-3940JCR Link
Citation
vol. 376, no. 3, pp. 171 - 176
Indexed
SCI; SCIE; SCOPUS scopus
Abstract
Recently we have reported that glucose deprivation induces the potentiated death and loss of ATP in immunostimulated astroglia via the production of NO and eventually peroxynitrite. This study examined the role of the ERK1/2 signaling pathways in the glucose deprivation-induced death of immunostimulated astroglia. Immunostimulation with LPS + IFN-γ induced the sustained activation of ERK1/2 for up to 48 h. Glucose deprivation caused the loss of ATP and consequently cell death in immunostimulated astroglia, which was significantly blocked by the treatment with the ERK kinase (MEK1) inhibitor, PD98059 (10-40 μM), to inhibit the ERK1/2 pathways. The systems for generating NO (iNOS) or superoxide (NADPH oxidase) were regulated by the ERK1/2 signaling pathways because the addition of PD98059 reduced the level of both. Interestingly, glucose deprivation caused an approximately two-fold increase in the level of peroxynitrite formation in immunostimulated astroglia, which was significantly reduced by the PD98059 treatment. This demonstrates that the ERK1/2 signaling pathways play an important role in glucose deprivation-induced death in immunostimulated astroglia by regulating the generation of NO, superoxide and their reaction product, peroxynitrite. © 2004 Elsevier Ireland Ltd. All rights reserved.
DOI
10.1016/j.neulet.2004.11.077
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자연과학대학 > 화학·나노과학전공 > Journal papers
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