Please use this identifier to cite or link to this item: http://hdl.handle.net/1942/18029
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dc.contributor.authorSlaets, Helena-
dc.contributor.authorNELISSEN, Sofie-
dc.contributor.authorJANSSENS, Kris-
dc.contributor.authorVIDAL VERA, Pia-
dc.contributor.authorLEMMENS, Evi-
dc.contributor.authorSTINISSEN, Piet-
dc.contributor.authorHENDRIX, Sven-
dc.contributor.authorHELLINGS, Niels-
dc.date.accessioned2014-12-18T15:58:38Z-
dc.date.available2014-12-18T15:58:38Z-
dc.date.issued2014-
dc.identifier.citationMOLECULAR NEUROBIOLOGY, 50 (3), p. 1142-1151-
dc.identifier.issn0893-7648-
dc.identifier.urihttp://hdl.handle.net/1942/18029-
dc.description.abstractThe family of interleukin (IL)-6 like cytokines plays an important role in the neuroinflammatory response to injury by regulating both neural as well as immune responses. Here, we show that expression of the IL-6 family member oncostatin M (OSM) and its receptor is upregulated after spinal cord injury (SCI). To reveal the relevance of increased OSM signaling in the pathophysiology of SCI, OSM was applied locally after spinal cord hemisection in mice. OSM treatment significantly improved locomotor recovery aftermild and severe SCI. Improved recovery in OSM treated mice was associated with a reduced lesion size. OSM significantly diminished astrogliosis and immune cell infiltration. Thus, OSM limits secondary damage after CNS trauma. In vitro viability assays demonstrated that OSM protects primary neurons in culture from cell death, suggesting that the underlying mechanism involves direct neuroprotective effects of OSM. Furthermore, OSM dose-dependently promoted neurite outgrowth in cultured neurons, indicating that the cytokine plays an additional role in CNS repair. Indeed, our in vivo experiments demonstrate that OSM treatment increases plasticity of serotonergic fibers after SCI. Together, our data show that OSMis produced at the lesion site, where it protects the CNS from further damage and promotes recovery.-
dc.description.sponsorshipThis work was financially supported by grants from NEURONET Methusalem and from the Flemish Fund for Scientific Research (FWO Vlaanderen) to H. S (1.5.121.12 N), to N. H. (G04441N), and to S. H. (G.0834.11 N, G.0389.12 N, G0A1413N).-
dc.language.isoen-
dc.publisherHUMANA PRESS INC-
dc.rights© Springer Science+Business Media New York 2014-
dc.subject.otherSCI; OSM; neuroinflammation; neuroprotection-
dc.subject.otherSCI; OSM; Neuroinflammation; Neuroprotection-
dc.titleOncostatin M Reduces Lesion Size and Promotes Functional Recovery and Neurite Outgrowth After Spinal Cord Injury-
dc.typeJournal Contribution-
dc.identifier.epage1151-
dc.identifier.issue3-
dc.identifier.spage1142-
dc.identifier.volume50-
local.format.pages10-
local.bibliographicCitation.jcatA1-
dc.description.notes[Slaets, Helena; Janssens, Kris; Stinissen, Piet; Hellings, Niels] Transnat Univ Limburg, Hasselt Univ, Biomed Res Inst, Sch Life Sci, Diepenbeek, Belgium. [Nelissen, Sofie; Vidal, Pia M.; Lemmens, Evi; Hendrix, Sven] Hasselt Univ, Dept Morphol, Diepenbeek, Belgium. [Nelissen, Sofie; Vidal, Pia M.; Lemmens, Evi; Hendrix, Sven] Hasselt Univ, Biomed Res Inst, B-3590 Diepenbeek, Belgium. [Nelissen, Sofie] Transnat Univ Limburg, B-3590 Diepenbeek, Belgium.-
local.publisher.placeTOTOWA-
local.type.refereedRefereed-
local.type.specifiedArticle-
dc.identifier.doi10.1007/s12035-014-8795-5-
dc.identifier.isi000344865700033-
item.fullcitationSlaets, Helena; NELISSEN, Sofie; JANSSENS, Kris; VIDAL VERA, Pia; LEMMENS, Evi; STINISSEN, Piet; HENDRIX, Sven & HELLINGS, Niels (2014) Oncostatin M Reduces Lesion Size and Promotes Functional Recovery and Neurite Outgrowth After Spinal Cord Injury. In: MOLECULAR NEUROBIOLOGY, 50 (3), p. 1142-1151.-
item.fulltextWith Fulltext-
item.accessRightsRestricted Access-
item.validationecoom 2015-
item.contributorVIDAL VERA, Pia-
item.contributorJANSSENS, Kris-
item.contributorSTINISSEN, Piet-
item.contributorNELISSEN, Sofie-
item.contributorHENDRIX, Sven-
item.contributorSlaets, Helena-
item.contributorLEMMENS, Evi-
item.contributorHELLINGS, Niels-
crisitem.journal.issn0893-7648-
crisitem.journal.eissn1559-1182-
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