title: c-Jun N-terminal kinase activation in hippocampal CA1 region was involved in ischemic injury.
abstract: To clarify the role of c-Jun N-terminal kinase (NK) activation in brain ischemia, temporospatial alteration of active (diphosphorylated) JNK1/2 immunoreactivity in hippocampus after brain ischemia in rat was investigated. Western immunoblot study showed that JNK1/2 diphosphorylation level was increased biphasically in CA1 but not CA3/dentate gyrus (DG) after 10 min of ischemia. Cerebral ventricular infusion of JNK1/2 antisense oligonucleotides not only significantly decreased JNK1/2 protein expression and the activation level but also significantly decreased CA1 pyramidal cell death (demonstrated by cresyl violet staining) and DNA fragmentation (demonstrated by in situ end-labeling of DNA). These results suggest that JNK1/2 were selectively activated and involved in the selective cell death in hippocampal CA1 subfield after cerebral ischemia.
authors: Research Center for Biochemistry and Molecular Biology, Xuzhou Medical College, PR China.
authors: Z
authors: Z
authors: Gu
authors: Q
authors: Q
authors: Jiang
authors: G
authors: G
authors: Zhang
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002545:Brain Ischemia / Q000201:enzymology* / Q000473:pathology; D002470:Cell Survival / Q000502:physiology; D004789:Enzyme Activation / Q000502:physiology; D006624:Hippocampus / Q000098:blood supply* / Q000201:enzymology* / Q000473:pathology; D007276:Injections, Intraventricular; D008297:Male; D048055:Mitogen-Activated Protein Kinase 8; D048056:Mitogen-Activated Protein Kinase 9; D020928:Mitogen-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D016376:Oligonucleotides, Antisense / Q000008:administration & dosage / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D016376:Oligonucleotides, Antisense; D048056:Mitogen-Activated Protein Kinase 9; D048055:Mitogen-Activated Protein Kinase 8; D020928:Mitogen-Activated Protein Kinases