title: Delayed induction of alpha B-crystallin in activated glia cells of hippocampus in kainic acid-treated mouse brain.
abstract: Small heat shock proteins have been implicated in playing a role in various cellular processes, including stress-induced cell death. In kainic acid (KA)-treated rat brain, the immunoreactivity of heat-shock protein 27 (HSP27) was markedly increased in glia cells of the limbic system. In the present study, we demonstrated that alpha B-crystallin, a member of the small heat-shock protein family, was strongly induced in reactive astrocytes in hippocampus after KA-induced seizure. The induction was localized mainly in the CA3 region of hippocampus, where massive neuronal loss occurred. We also demonstrated that the delayed induction of alpha B-crystallin and HSP27 immunoreactivities in the hippocampus of epileptic animals was repressed to the levels seen in control animals with preadministration of the selective nNOS inhibitor 7-nitroindazole (7-NI). This repression was reversed by coinjection of L-arginine, a substrate of NOS. Together, these data suggest a role for alpha B-crystallin and HSP27 in reactive gliosis and/or in delayed neuronal death proceeded after KA-induced seizure.
authors.affiliation: Department of Anatomy, Inha University School of Medicine, Inchon, Korea.
authors.forename: Y
authors.initials: Y
authors.lastname: Che
authors.forename: C S
authors.initials: CS
authors.lastname: Piao
authors.forename: P L
authors.initials: PL
authors.lastname: Han
authors.forename: J K
authors.initials: JK
authors.lastname: Lee
mesh_terms: D000818:Animals; D001120:Arginine / Q000494:pharmacology; D001253:Astrocytes / Q000187:drug effects / Q000378:metabolism* / Q000473:pathology; D003459:Crystallins / Q000187:drug effects / Q000378:metabolism*; D004347:Drug Interactions / Q000502:physiology; D004791:Enzyme Inhibitors / Q000494:pharmacology; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D005911:Gliosis / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D006360:Heat-Shock Proteins; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D007150:Immunohistochemistry; D007191:Indazoles / Q000494:pharmacology; D007608:Kainic Acid / Q000494:pharmacology; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D018832:Molecular Chaperones; D009363:Neoplasm Proteins / Q000187:drug effects / Q000378:metabolism*; D009410:Nerve Degeneration / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D018696:Neuroprotective Agents / Q000494:pharmacology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D012640:Seizures / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*
chemical_list: D003459:Crystallins; D004791:Enzyme Inhibitors; D018690:Excitatory Amino Acid Agonists; D006360:Heat-Shock Proteins; C486113:Hsbp1 protein, mouse; D007191:Indazoles; D018832:Molecular Chaperones; D009363:Neoplasm Proteins; D018696:Neuroprotective Agents; D009569:Nitric Oxide; D001120:Arginine; D019001:Nitric Oxide Synthase; D007608:Kainic Acid; C080122:7-nitroindazole