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Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/19071

Title: Oncostatin M protects against demyelination by inducing a protective microglial phenotype.
Authors: Janssens, Kris
Maheshwari, Anurag
Van den Haute, C.
Baekelandt, Veerle
Stinissen, Piet
Hendriks, Jerome
Slaets, Leen
Hellings, Niels
Issue Date: 2015
Citation: GLIA, 63 (10), p. 1729-1737
Abstract: Multiple sclerosis (MS) is a chronic disabling disease of the central nervous system (CNS), in which destruction of myelin sheaths leads to disturbed axonal conduction. Available MS therapies modulate the immune response, but are unable to prevent neurological decline. Therefore, great efforts are made to develop therapies that limit demyelination and axonal degeneration. Oncostatin M (OSM), a member of the interleukin (IL)-6 cytokine family, is produced in demyelinating lesions of MS patients and stimulates neuronal survival. In this study, we reveal that the OSM receptor (OSMR) was robustly upregulated on microglia/macrophages and astrocytes in the cuprizone-induced demyelination model. While OSMR deficiency led to aggravated demyelination, CNS-targeted OSM treatment largely prevented demyelination. OSM treatment increased IL-4 expression and induced polarization of myeloid cells towards an anti-inflammatory M2 phenotype in vivo. This study reveals a previously uncharacterized and protective role for OSM during demyelination, and indicates that OSM is a promising therapeutic candidate to limit CNS damage in demyelinating diseases including MS
Notes: Address correspondence to Niels Hellings, Agoralaan building C, 3590 Diepenbeek, Belgium. E-mail: niels.hellings@uhasselt.be
URI: http://hdl.handle.net/1942/19071
DOI: 10.1002/glia.22840
ISI #: 000359606700004
ISSN: 0894-1491
Category: A1
Type: Journal Contribution
Validation: ecoom, 2016
Appears in Collections: Research publications

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