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Trail interacts redundantly with nitric oxide in rat astrocytes: Potential contribution to neurodegenerative processes

被引：25
作者：
Cantarella, Giuseppina
Lempereur, Laurence
D'Alcamo, Maria Antonia
Risuglia, Nunziata
Cardile, Vera
Pennisi, Giuseppa
Scoto, Glovanna Maria
Bernardini, Renato
机构：
[1] Catania Univ, Dept Expt & Clin Pharmacol, I-95125 Catania, Italy
[2] Univ Catania, Dept Physiol Sci, I-95125 Catania, Italy
[3] Univ Catania, Dept Chem Sci, I-95125 Catania, Italy
[4] Catania Univ, Dept Pharmaceut Sci, I-95125 Catania, Italy
来源：
JOURNAL OF NEUROIMMUNOLOGY | 2007年 / 182卷 / 1-2期
关键词：
glia; neuroinflammation; proapoptotic cytokines; oxidative stress; neurodegeneration;
D O I：
10.1016/j.jneuroim.2006.09.007
中图分类号：
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号：
100102 [免疫学];
摘要：
The proapoptotic cytokine TRAIL has been shown to enhance amyloid-beta-dependent neurotoxicity. Here are reported interactions between TRAIL and nitric oxide (NO) in cultured rat astrocytes in vitro. Rat astrocytes expressed all TRAIL receptor mRNAs and proteins. However, TRAIL failed in inducing apoptosis of astrocytes, whereas these cells released substantial amounts of nitrites. A TRAIL-neutralizing antibody was able to prevent LPS-induced iNOS expression in astrocytes. Interestingly, TRAIL induced its own expression in astrocytes. These data suggest that redundancy between TRAIL and NO in astrocytes could be fueling neuronal damage/death processes, potentially uncovering novel molecular targets for the treatment of neurodegenerative disorders. (c) 2006 Elsevier B.V. All rights reserved.
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页码：41 / 47
页数：7
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