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Title

FGF-2 and anosmin-1 are selectively expressed in different types of multiple sclerosis lesions

AuthorsClemente, Diego; Ortega, M.C.; Arenzana, F.J.; Castro Soubriet, Fernando de
KeywordsFGF-2
Multiple sclerosis
Issue Date2011
PublisherSociety for Neuroscience
CitationJournal of Neuroscience 31: 14899- 14909 (2011)
AbstractMultiple sclerosis is a demyelinating disease that affects ~2,000,000 people worldwide. In the advanced stages of the disease, endogenous oligodendrocyte precursors cannot colonize the lesions or differentiate into myelinating oligodendrocytes. During development, both FGF-2 and Anosmin-1 participate in oligodendrocyte precursor cell migration, acting via the FGF receptor 1 (FGFR1). Hence, we performed a histopathological and molecular analysis of these developmental modulators in postmortem tissue blocks from multiple sclerosis patients. Accordingly, we demonstrate that the distribution of FGF-2 and Anosmin-1 varies between the different types of multiple sclerosis lesions: FGF-2 is expressed only within active lesions and in the periplaque of chronic lesions, whereas Anosmin-1 is upregulated within chronic lesions and is totally absent in active lesions. We show that the endogenous oligodendrocyte precursor cells recruited toward chronic-active lesions express FGFR1, possibly in response to the FGF-2 produced by microglial cells in the periplaque. Also in human tissue, FGF-2 is upregulated in perivascular astrocytes in regions of the normal-appearing gray matter, where the integrity of the blood-brain barrier is compromised. In culture, FGF-2 and Anosmin-1 influence adult mouse oligodendrocyte precursor cell migration in the same manner as at embryonic stages, providing an explanation for the histopathological observations: FGF-2 attracts/ enhances its migration, which is hindered by Anosmin-1. We propose that FGF-2 and Anosmin-1 are markers for the histopathological type and the level of inflammation of multiple sclerosis lesions, and that they may serve as novel pharmacogenetic targets to design future therapies that favor effective remyelination and protect the blood-brain barrier. © 2011 the authors.
URIhttp://hdl.handle.net/10261/156755
DOI10.1523/JNEUROSCI.1158-11.2011
Identifiersdoi: 10.1523/JNEUROSCI.1158-11.2011
issn: 0270-6474
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