Diphosphorylation of extracellular signal-regulated kinases and c-Jun N-terminal protein kinases in brain ischemic tolerance in rat.
Extracellular signal-regulated kinases (ERKs) and c-Jun N-terminal protein kinases (JNKs) activation in brain ischemic tolerance were examined by Western immunoblot. ERK but not JNK diphosphorylation (activation) were increased after preconditioning ischemia. The increased JNK1 but not ERK diphosphorylation after lethal ischemia was eliminated by pretreatment with preconditioning ischemia. The results suggest that the elimination of JNK1 activation after lethal ischemia by preconditioning ischemia may be one of the important protective mechanisms in ischemic tolerance, and ERKs activation may be involved in the induction of the protective responses.
Gu
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Research Center of Biochemistry and Molecular Biology, Xuzhou Medical College, Xuzhou, China. gyzhang@xzmc.edu.cn
Jiang
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Zhang
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Cui
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Zhu
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D000818:Animals; D001925:Brain Damage, Chronic / Q000209:etiology / Q000517:prevention & control*; D002545:Brain Ischemia / Q000150:complications / Q000201:enzymology*; D002452:Cell Count; D004789:Enzyme Activation; D006624:Hippocampus / Q000201:enzymology / Q000473:pathology; D019194:Ischemic Preconditioning; D048031:JNK Mitogen-Activated Protein Kinases; D008297:Male; D019950:Mitogen-Activated Protein Kinase 1 / Q000378:metabolism*; D048052:Mitogen-Activated Protein Kinase 3; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D009419:Nerve Tissue Proteins / Q000378:metabolism*; D009474:Neurons / Q000473:pathology; D010766:Phosphorylation; D011499:Protein Processing, Post-Translational; D051381:Rats; D017207:Rats, Sprague-Dawley
D009419:Nerve Tissue Proteins; D048031:JNK Mitogen-Activated Protein Kinases; D019950:Mitogen-Activated Protein Kinase 1; D048052:Mitogen-Activated Protein Kinase 3; D020928:Mitogen-Activated Protein Kinases