Potentiated glucose deprivation-induced death of astrocytes after induction of iNOS.
Astrocytes play an essential role in the maintenance of normal neuronal function. Here we report that pretreatment of interferon-gamma (IFN-gamma) and lipopolysaccharides (LPS) made murine astrocytes highly vulnerable to glucose deprivation-induced death. Neither 12-hr glucose deprivation nor 2-day treatment with IFN-gamma (100 U/ml) and LPS (1 microg/ml) altered the viability of astrocytes. However, significant death of IFN-gamma/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 NG-nitroarginine. The data indicate that immunostimulated astrocytes can undergo suicidal death during glucose deprivation through the expression of inducible nitric oxide synthase.
Choi
J J
JJ
Department of Pharmacology, College of Medicine, Ewha Women's University, Seoul, Republic of Korea.
Kim
W K
WK
D000818:Animals; D001253:Astrocytes / Q000187:drug effects* / Q000201:enzymology; D016923:Cell Death / Q000187:drug effects*; D003470:Culture Media; D004790:Enzyme Induction; D005947:Glucose / Q000008:administration & dosage* / Q000378:metabolism; D007371:Interferon-gamma / Q000494:pharmacology*; D008070:Lipopolysaccharides / Q000494:pharmacology*; D009569:Nitric Oxide / Q000378:metabolism*; D019001:Nitric Oxide Synthase / Q000378:metabolism*; D052247:Nitric Oxide Synthase Type II; D051381:Rats; D017207:Rats, Sprague-Dawley
D003470:Culture Media; D008070:Lipopolysaccharides; D009569:Nitric Oxide; D007371:Interferon-gamma; D019001:Nitric Oxide Synthase; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D005947:Glucose