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Potentiated glucose deprivation‐induced death of astrocytes after induction of iNOS
Author(s) -
Choi JungJin,
Kim WonKi
Publication year - 1998
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/(sici)1097-4547(19981215)54:6<870::aid-jnr15>3.0.co;2-3
Subject(s) - nitric oxide synthase , nitric oxide , astrocyte , programmed cell death , chemistry , endocrinology , medicine , lipopolysaccharide , apoptosis , biology , biochemistry , central nervous system
Astrocytes play an essential role in the maintenance of normal neuronal function. Here we report that pretreatment of interferon‐γ (IFN‐γ) and lipopolysaccharides (LPS) made murine astrocytes highly vulnerable to glucose deprivation‐induced death. Neither 12‐hr glucose deprivation nor 2‐day treatment with IFN‐γ (100 U/ml) and LPS (1 μg/ml) altered the viability of astrocytes. However, significant death of IFN‐γ/LPS‐treated astrocytes was observed after 4‐hr glucose deprivation. This augmented death was mimicked by the nitric oxide releasing reagent 3‐morpholinosydnonimine and was in part prevented by the nitric oxide synthase inhibitor N G ‐nitroarginine. The data indicate that immunostimulated astrocytes can undergo suicidal death during glucose deprivation through the expression of inducible nitric oxide synthase. J. Neurosci. Res. 54:870–875, 1998. © 1998 Wiley‐Liss, Inc.