NDLI: The EIIIA domain from astrocyte‐derived fibronectin mediates proliferation of oligodendrocyte progenitor cells following CNS demyelination

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The EIIIA domain from astrocyte‐derived fibronectin mediates proliferation of oligodendrocyte progenitor cells following CNS demyelination

Content Provider	PubMed Central
Author	Stoffels, Josephine M. J. Hoekstra, Dick Franklin, Robin J. M. Baron, Wia Zhao, Chao
Abstract	Central nervous system remyelination by oligodendrocyte progenitor cells (OPCs) ultimately fails in the majority of multiple sclerosis (MS) lesions. Remyelination benefits from transient expression of factors that promote migration and proliferation of OPCs, which may include fibronectin (Fn). Fn is present in demyelinated lesions in two major forms; plasma Fn (pFn), deposited following blood‐brain barrier disruption, and cellular Fn, synthesized by resident glial cells and containing alternatively spliced domains EIIIA and EIIIB. Here, we investigated the distinctive roles that astrocyte‐derived Fn (aFn) and pFn play in remyelination. We used an inducible Cre‐lox recombination strategy to selectively remove pFn, aFn or both from mice, and examined the impact on remyelination of toxin‐induced demyelinated lesions of spinal cord white matter. This approach revealed that astrocytes are a major source of Fn in demyelinated lesions. Furthermore, following aFn conditional knockout, the number of OPCs recruited to the demyelinated lesion decreased significantly, whereas OPC numbers were unaltered following pFn conditional knockout. However, remyelination completed normally following conditional knockout of aFn and pFn. Both the EIIIA and EIIIB domains of aFn were expressed following demyelination, and in vitro assays demonstrated that the EIIIA domain of aFn mediates proliferation of OPCs, but not migration. Therefore, although the EIIIA domain from aFn mediates OPC proliferation, aFn is not essential for successful remyelination. Since previous findings indicated that astrocyte‐derived Fn aggregates in chronic MS lesions inhibit remyelination, aFn removal may benefit therapeutic strategies to promote remyelination in MS. GLIA 2015;63:242–256
Related Links	http://dx.doi.org/10.1002/glia.22748
Ending Page	256
Page Count	15
Starting Page	242
File Format	PDF
ISSN	08941491
e-ISSN	10981136
Journal	Glia
Issue Number	2
Volume Number	63
Language	English
Publisher	John Wiley and Sons Inc.
Publisher Date	2015-02-01
Access Restriction	Open
Rights Holder	John Wiley and Sons Inc.
Subject Keyword	Cellular and Molecular Neuroscience Neurology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Neurology Cellular and Molecular Neuroscience

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