Induction of intracellular ceramide by interleukin-1β in oligodendrocytes

The sphingomyelin pathway has been implicated in mediating the effect of several extracellular agents leading to important biochemical and cellular changes. The aim of this investigation is to study interleukin‐1β (IL‐1β) signaling in oligodendrocytes. For this purpose, the CG4 oligodendrocyte cells...

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Published in:Journal of cellular biochemistry Vol. 66; no. 4; pp. 532 - 541
Main Authors: Brogi, Alessandra, Strazza, Michelina, Melli, Marialuisa, Costantino-Ceccarini, Elvira
Format: Journal Article
Language:English
Published: Hoboken Wiley Subscription Services, Inc., A Wiley Company 15-09-1997
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Summary:The sphingomyelin pathway has been implicated in mediating the effect of several extracellular agents leading to important biochemical and cellular changes. The aim of this investigation is to study interleukin‐1β (IL‐1β) signaling in oligodendrocytes. For this purpose, the CG4 oligodendrocyte cells were differentiated and incubated with IL‐1β. This treatment induced a time‐ and dose‐dependent increase of the endocellular ceramide. To mimic the effect of the elevation of endogenous ceramide, the CG4 cells were treated with the ceramide analogue C2‐ceramide. Cell survival, measured with the MTT assay, showed that, by increasing the concentration of ceramide, up to 40% of CG4 cells were dying within 6 h, similar data were obtained with the primary differentiated oligodendrocytes. Condensation of chromatin, nuclear fragmentation, and formation of apoptotic bodies indicated that apoptosis was the cause of death. Surprisingly, long‐term exposure (72 h) to increasing concentrations of IL‐1β, which increases intracellular ceramide, did not induce oligodendroglial cell death. These results show that an increase of intracellular ceramide is not sufficient to induce apoptosis in oligodendrocytes and that IL‐1β signaling through the ceramide pathway in these cells can mediate functions other than programmed cell death. J. Cell Biochem. 66:532–541, 1997. © 1997 Wiley‐Liss, Inc.
Bibliography:ark:/67375/WNG-L7C47LW0-T
ArticleID:JCB12
istex:12A4E221905ADCD55B278D61F0020A9FC3C380E0
Istituto Superiore di Sanità, Multiple Sclerosis Project
ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:0730-2312
1097-4644
DOI:10.1002/(SICI)1097-4644(19970915)66:4<532::AID-JCB12>3.0.CO;2-D