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Delayed induction of αB-crystallin in activated glia cells of hippocampus in kainic acid-treated mouse brain
- Delayed induction of αB-crystallin in activated glia cells of hippocampus in kainic acid-treated mouse brain
- Che Y.; Piao C.S.; Han P.-L.; Lee J.-K.
- Ewha Authors
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- Journal of Neuroscience Research
- Journal of Neuroscience Research vol. 65, no. 5, pp. 425 - 431
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- 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 αB-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 αB-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 αB-crystallin and HSP27 in reactive gliosis and/or in delayed neuronal death proceeded after KA-induced seizure. © 2001 Wiley-Liss, Inc.
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