Biphasic activation of apoptosis signal-regulating kinase 1-stress-activated protein kinase 1-c-Jun N-terminal protein kinase pathway is selectively mediated by Ca2+-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors involving oxidative stress following brain ischemia in rat hippocampus

Quanguang Zhang, Guangyi Zhang, Fanjie Meng, Hui Tian

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Stress-activated protein kinase/extracellular signal-regulated kinase-1 (SEK1/MKK4) was examined in a rat model of global brain ischemia. Western blot assay showed that SEK1 activation was biphasic in CA1 but not CA3/dentate gyrus. The second activation peak (3 days after ischemia) was prevented by pretreatment with l-naphthyl acetyl spermine (Naspm), a channel blocker of Ca2+-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors, or N-acetylcysteine (NAC), a free radical scavenger. Concomitantly, the late activation of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal protein kinase (JNK) was also prevented by Naspm or NAC. Moreover, phospho-SEK1 and phospho-JNK co-immunoprecipitated with ASK1 and the bindings peaked at 3 days of reperfusion. Together with previous results, these findings indicate that Ca2+-permeable AMPA receptors are important routes to mediate the late activation of ASK1-SEK1-JNK pathway involving oxidative stress in hippocampal CA1 region after ischemia.

Original languageEnglish (US)
Pages (from-to)51-55
Number of pages5
JournalNeuroscience Letters
Volume337
Issue number1
DOIs
StatePublished - Jan 30 2003

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MAP Kinase Kinase Kinase 5
Mitogen-Activated Protein Kinase 8
JNK Mitogen-Activated Protein Kinases
Brain Ischemia
Hippocampus
Oxidative Stress
AMPA Receptors
Spermine
Acetylcysteine
Ischemia
Hippocampal CA1 Region
Free Radical Scavengers
Proteins
Mitogen-Activated Protein Kinase 3
MAP Kinase Signaling System
Dentate Gyrus
Heat-Shock Proteins
Protein Kinases
Reperfusion
Western Blotting

Keywords

  • Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors
  • Apoptosis signal-regulating kinase 1
  • Brain ischemia
  • Hippocampus
  • L-naphthyl acetyl spermine
  • N-acetylcysteine
  • Rat
  • Stress-activated protein kinase-1
  • c-Jun N-terminal protein kinase

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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title = "Biphasic activation of apoptosis signal-regulating kinase 1-stress-activated protein kinase 1-c-Jun N-terminal protein kinase pathway is selectively mediated by Ca2+-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors involving oxidative stress following brain ischemia in rat hippocampus",
abstract = "Stress-activated protein kinase/extracellular signal-regulated kinase-1 (SEK1/MKK4) was examined in a rat model of global brain ischemia. Western blot assay showed that SEK1 activation was biphasic in CA1 but not CA3/dentate gyrus. The second activation peak (3 days after ischemia) was prevented by pretreatment with l-naphthyl acetyl spermine (Naspm), a channel blocker of Ca2+-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors, or N-acetylcysteine (NAC), a free radical scavenger. Concomitantly, the late activation of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal protein kinase (JNK) was also prevented by Naspm or NAC. Moreover, phospho-SEK1 and phospho-JNK co-immunoprecipitated with ASK1 and the bindings peaked at 3 days of reperfusion. Together with previous results, these findings indicate that Ca2+-permeable AMPA receptors are important routes to mediate the late activation of ASK1-SEK1-JNK pathway involving oxidative stress in hippocampal CA1 region after ischemia.",
keywords = "Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors, Apoptosis signal-regulating kinase 1, Brain ischemia, Hippocampus, L-naphthyl acetyl spermine, N-acetylcysteine, Rat, Stress-activated protein kinase-1, c-Jun N-terminal protein kinase",
author = "Quanguang Zhang and Guangyi Zhang and Fanjie Meng and Hui Tian",
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T1 - Biphasic activation of apoptosis signal-regulating kinase 1-stress-activated protein kinase 1-c-Jun N-terminal protein kinase pathway is selectively mediated by Ca2+-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate receptors involving oxidative stress following brain ischemia in rat hippocampus

AU - Zhang, Quanguang

AU - Zhang, Guangyi

AU - Meng, Fanjie

AU - Tian, Hui

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AB - Stress-activated protein kinase/extracellular signal-regulated kinase-1 (SEK1/MKK4) was examined in a rat model of global brain ischemia. Western blot assay showed that SEK1 activation was biphasic in CA1 but not CA3/dentate gyrus. The second activation peak (3 days after ischemia) was prevented by pretreatment with l-naphthyl acetyl spermine (Naspm), a channel blocker of Ca2+-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptors, or N-acetylcysteine (NAC), a free radical scavenger. Concomitantly, the late activation of apoptosis signal-regulating kinase 1 (ASK1) and c-Jun N-terminal protein kinase (JNK) was also prevented by Naspm or NAC. Moreover, phospho-SEK1 and phospho-JNK co-immunoprecipitated with ASK1 and the bindings peaked at 3 days of reperfusion. Together with previous results, these findings indicate that Ca2+-permeable AMPA receptors are important routes to mediate the late activation of ASK1-SEK1-JNK pathway involving oxidative stress in hippocampal CA1 region after ischemia.

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