| Literature DB >> 17067687 |
Giuseppina Cantarella1, Laurence Lempereur, Maria Antonia D'Alcamo, Nunziata Risuglia, Vera Cardile, Giuseppa Pennisi, Giovanna Maria Scoto, Renato Bernardini.
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.Entities:
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Year: 2006 PMID： 17067687 DOI： 10.1016/j.jneuroim.2006.09.007
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478