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

Byoung Kwon Yoo, Ji Woong Choi, Byoung Hee Han, Won Ki Kim, Hyoung Chun Kim, Kwang Ho Ko

Research output: Contribution to journalArticle

24 Citations (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.

Original languageEnglish
Pages (from-to)171-176
Number of pages6
JournalNeuroscience Letters
Volume376
Issue number3
DOIs
Publication statusPublished - 2005 Mar 16
Externally publishedYes

Keywords

  • ERK1/2
  • Glucose deprivation
  • Immunostimulated astroglia
  • Peroxynitrite

ASJC Scopus subject areas

  • Neuroscience(all)

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