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XIAP protects oligodendrocytes against cell death in vitro but has no functional role in toxic demyelination
Author(s) -
Rena Hesse Amke,
Hagemeier Karin,
Lürbke Alexander,
Held Jasmin,
Friedman Hana,
Peterson Alan,
Brück Wolfgang,
Kuhlmann Tanja
Publication year - 2012
Publication title -
glia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.954
H-Index - 164
eISSN - 1098-1136
pISSN - 0894-1491
DOI - 10.1002/glia.21261
Subject(s) - xiap , biology , neuroprotection , myelin , programmed cell death , multiple sclerosis , apoptosis , oligodendrocyte , inhibitor of apoptosis , in vivo , microbiology and biotechnology , neuroscience , immunology , caspase , central nervous system , biochemistry , genetics
Abstract Oligodendroglial damage and loss are typical characteristics of demyelinating diseases such as multiple sclerosis (MS) and the leukodystrophies. Axonal loss is the underlying cause of permanent neurological deficits in MS and it is thought to arise from a combination of immune‐mediated axonal damage and the loss of trophic support to axons from myelin sheaths after demyelination. Prevention of oligodendroglial damage or death and demyelination are therefore attractive neuroprotective treatment strategies. However, a better understanding of mechanisms leading to oligodendroglial damage and demyelination is a prerequisite for the development of such treatment options. Here, we demonstrate that X‐linked inhibitor of apoptosis (XIAP), the most potent member of the inhibitor of apoptosis proteins (IAP) family is expressed in oligodendrocytes in vivo and in vitro . Increased expression of XIAP is associated with protection against selected cell death pathways, whereas decreased expression increases oligodendroglial cell death in vitro . However, lack of XIAP does not modulate oligodendroglial cell death in toxic demyelination in vivo . © 2011 Wiley Periodicals, Inc.