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Immunostimulated glial cells potentiate glucose deprivation-induced death of cultured rat cerebellar granule cells

Title
Immunostimulated glial cells potentiate glucose deprivation-induced death of cultured rat cerebellar granule cells
Authors
Kim W.-K.Seo D.O.Choi J.-J.Ko K.H.
Ewha Authors
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Issue Date
1999
Journal Title
Journal of Neurotrauma
ISSN
0897-7151JCR Link
Citation
vol. 16, no. 5, pp. 415 - 424
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
The present study investigates whether immunostimulated glial expression of inducible nitric oxide synthase influences the glucose deprivation- induced death of rat cerebellar granule cells (CGC). CGC/glia cocultures were immunostimulated by interferon-γ (200 U/ml) and lipopolysaccharides (1 μg/ml) and 2 days later were challenged by glucose deprivation. Neurotoxicity was assessed by measuring the release of lactate dehydrogenase. Neither a 2-h glucose deprivation nor a 2-day immunostimulation altered the viability of CGC. A 2-day immunostimulation, however, markedly potentiated the glucose deprivation-induced death of CGC. The increased death of glucose- deprived CGC after immunostimulation was mimicked by the nitric oxide (NO) releasing reagent 3-morpholinosydnonimine (SIN-1) and was partially prevented by the NO synthase (NOS) inhibitor N(G)-nitroarginine. The increased death of glucose-deprived CGC either after immunostimulation or by SIN-1 was not altered by various N-methyl-D-aspartate (NMDA) and non-NMDA receptor antagonists. Because superoxide dismutase and catalase, which remove superoxide anion, decreased the augmented death of glucose-deprived immunostimulated CGC, the reaction of NO with superoxide to form peroxynitrite appears to be implicated in the potentiated neurotoxicity. Our data indicate that immunostimulated glial cells potentiate the death of glucose-deprived neurons in part through the expression of inducible NOS but not through NMDA receptor activation. Potentiation of glucose-deprived CGC death by immunostimulated glial cells may be clinically implicated in the tendency of recurrent ischemic insults to be more severe and fatal than an initial ischemic insult.
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자연과학대학 > 화학·나노과학전공 > Journal papers
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