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Tumor necrosis factor‐α and αB‐crystallin up‐regulation during antibody‐mediated demyelination in vitro: A putative protective mechanism in oligodendrocytes
Author(s) -
Duvanel Cécile Besson,
MonnetTschudi Florianne,
Braissant Olivier,
Matthieu JeanMarie,
Honegger Paul
Publication year - 2004
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20310
Subject(s) - oligodendrocyte , tumor necrosis factor alpha , heat shock protein , biology , apoptosis , myelin oligodendrocyte glycoprotein , myelin , microbiology and biotechnology , programmed cell death , antibody , immunology , in vitro , microglia , neuroprotection , inflammation , neuroscience , central nervous system , gene , biochemistry
By using an in vitro model of antibody‐mediated demyelination, we investigated the relationship between tumor necrosis factor‐α (TNF‐α) and heat shock protein (HSP) induction with respect to oligodendrocyte survival. Differentiated aggregate cultures of rat telencephalon were subjected to demyelination by exposure to antibodies against myelin oligodendrocyte glycoprotein (MOG) and complement. Cultures were analyzed 48 hr after exposure. Myelin basic protein (MBP) expression was greatly decreased, but no evidence was found for either necrosis or apoptosis. TNF‐α was significantly up‐regulated. It was localized predominantly in neurons and to a lesser extent in astrocytes and oligodendrocytes, and it was not detectable in microglial cells. Among the different HSPs examined, HSP32 and αB‐crystallin were up‐regulated; they may confer protection from oxidative stress and from apoptotic death, respectively. These results suggest that TNF‐α, often regarded as a promoter of oligodendroglial death, could alternatively mediate a protective pathway through αB‐crystallin up‐regulation. © 2004 Wiley‐Liss, Inc.