| XIAP protects oligodendrocytes against cell death in vitro but has no functional role in toxic demyelination. | |
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MedLine Citation:
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PMID: 22065417 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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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. |
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Authors:
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Amke Rena Hesse; Karin Hagemeier; Alexander Lürbke; Jasmin Held; Hana Friedman; Alan Peterson; Wolfgang Brück; Tanja Kuhlmann |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-11-7 |
Journal Detail:
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Title: Glia Volume: - ISSN: 1098-1136 ISO Abbreviation: - Publication Date: 2011 Nov |
Date Detail:
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Created Date: 2011-11-8 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8806785 Medline TA: Glia Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2011 Wiley-Liss, Inc. |
Affiliation:
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Institute of Neuropathology, University Hospital Münster, Domagkstr. 19, Münster, Germany. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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