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J Neuroimmunol. 2007 Jan;182(1-2):41-7. Epub 2006 Oct 24.

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

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  • 1Department of Experimental and Clinical Pharmacology, University of Catania, Viale Andrea Doria, 6, I-95125 Catania, Italy.

Abstract

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.

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