Osteopontin is extensively expressed by macrophages following CNS demyelination but has a redundant role in remyelination

Zhao, Chao, Fancy, Stephen P.J., ffrench-Constant, Charles ORCID: https://orcid.org/0000-0002-5621-3377 and Franklin, Robin J.M. (2008) Osteopontin is extensively expressed by macrophages following CNS demyelination but has a redundant role in remyelination. Neurobiology of Disease, 31 (2). pp. 209-217. ISSN 0969-9961

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Abstract

Osteopontin (OPN) is a key immunoregulator in the autoimmune-mediated demyelinating disease multiple sclerosis. OPN may also play a role in the remyelination since it is 1) a ligand for αV integrins, several of which regulate the properties of the oligodendrocyte precursor cells (OPCs) primarily responsible for remyelination, and 2) enhances myelin membrane formation in OPC lines. Here we show that OPN is expressed at high levels during remyelination of toxin-induced demyelination. The increased expression is due to mRNA expression in macrophages and follows differences in macrophage responses to demyelination in young and old adult animals. To identify the role of OPN in remyelination focal demyelination was induced in wild-type and OPN-/- mice. There was no difference in the rate of remyelination between the two groups indicating that OPN is not a critical component of remyelination.

Item Type: Article
Additional Information: Funding Information: This work was supported by grants from the UK Multiple Sclerosis Society. We are very grateful to Michael Peacock for his excellent technical assistance. We are also very grateful to Dr Susan Rittling for the donation of the OPN −/− mice.
Uncontrolled Keywords: demyelination,knockout,multiple sclerosis,myelin,oligodendrocyte precursor cell,osteopontin,regeneration,remyelination,neurology ,/dk/atira/pure/subjectarea/asjc/2800/2808
Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
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Depositing User: LivePure Connector
Date Deposited: 16 Jul 2022 11:30
Last Modified: 13 Aug 2022 02:21
URI: https://ueaeprints.uea.ac.uk/id/eprint/86310
DOI: 10.1016/j.nbd.2008.04.007

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