Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/10284
Title: ONCOSTATIN M IS A POTENT INDUCER OF CNS INFLAMMATION
Authors: Slaets, Leen 
Hendriks, Jerome 
de Vries, H.
Van den Haute, C.
Baekelandt, Veerle
Stinissen, Piet 
Hellings, Niels 
Issue Date: 2009
Publisher: WILEY-LISS
Source: GLIA, 57(13). p. S138-S138
Abstract: The neuropoietic cytokine oncostatin M (OSM) is expressed in MS lesions, but its function during CNS lesion development is unknown. We have induced local expression of OSM in the CNS of C57Bl/6J mice by means of lentiviral vectors. Our data demonstrate that at sites of OSM expression, tissue remodelling occurs and an irregular deposition of the basement membrane protein laminin is detected. Further analysis demonstrated that local OSM expression disrupts several aspects of the blood-brain barrier (BBB): large perivascular spaces were found between the inner and outer basement membranes, expression of the tight junction protein ZO-1 was altered and serum leaks into the CNS parenchyma. In addition, local OSM expression induced an upregulation of adhesion molecules on endothelial cells of the BBB. Moreover, OSM-expression was accompanied by an upregulation of MHCII molecules and an infiltration of T-cells and macrophages/microglia into the brain. This is the first study demonstrating that local OSM expression in the healthy CNS is sufficient to induce several aspects charateristic of neuroinflammation.
Notes: [Slaets, H.; Hendriks, J.; Stinissen, P.; Hellings, N.] Hasselt Univ, Diepenbeek, Belgium. [de Vries, H.] Vrije Univ Amsterdam Med Ctr, Amsterdam, Netherlands. [Van den Haute, C.; Baekelandt, V] Katholieke Univ Leuven, Louvain, Belgium.
Keywords: neurosciences
Document URI: http://hdl.handle.net/1942/10284
ISSN: 0894-1491
e-ISSN: 1098-1136
ISI #: 000270075500570
Category: M
Type: Journal Contribution
Appears in Collections:Research publications

Show full item record

Page view(s)

14
checked on May 18, 2022

Google ScholarTM

Check


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.