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dc.contributor.authorSlevin, Mark
dc.contributor.authorKrupinski, Jerzy
dc.contributor.authorMitsios, Nick
dc.contributor.authorPerikleous, C
dc.contributor.authorCuadrado, E
dc.contributor.authorMontaner, J
dc.contributor.authorSanfeliu, Coral
dc.contributor.authorLuque, A
dc.contributor.authorKumar, Shant
dc.contributor.authorKumar, Patricia
dc.contributor.authorGaffney, John
dc.date.accessioned2009-05-14T13:45:39Z
dc.date.available2009-05-14T13:45:39Z
dc.date.issued2008-01
dc.identifier.citationLeukaemia inhibitory factor is over-expressed by ischaemic brain tissue concomitant with reduced plasma expression following acute stroke. 2008, 15 (1):29-37 Eur. J. Neurol.en
dc.identifier.issn1468-1331
dc.identifier.pmid18042242
dc.identifier.doi10.1111/j.1468-1331.2007.01995.x
dc.identifier.urihttp://hdl.handle.net/10541/68193
dc.description.abstractLeukaemia inhibitory factor (LIF) is a glycoprotein of the interleukin-6 family, which has potent pro-inflammatory properties and is involved in regulation of neuronal differentiation. We have previously identified its upregulation in gene microarrays following acute ischaemic stroke in man. LIF expression and localization was measured in human ischaemic stroke autopsy specimens, in a rat model of middle cerebral artery occlusion (MCAO) and in human foetal neural cell cultures following oxygen-glucose deprivation (OGD) by Western blotting and immunohistochemistry. Circulating LIF was determined in the plasma of patients in the hyper-acute stroke phase using a multiplex enzyme-linked-immunosorbent serologic assay system. Patients demonstrated an increase in LIF expression in peri-infarcted regions with localization in neurons and endothelial cells of microvessels surrounding the infarcted core. The rat MCAO model showed similar upregulation in neurons with a peak increase at 90 min. Circulating serum LIF expression was significantly decreased in the hyper-acute phase of stroke. Brain-derived neurons and glia cultured in vitro demonstrated an increase in gene/protein and protein expression respectively following exposure to OGD. Increased LIF expression in peri-infarcted regions and sequestration from the peripheral circulation in acute stroke patients are characteristic of the pathobiological response to ischaemia and tissue damage.
dc.language.isoenen
dc.subjectGliaen
dc.subjectIschaemic Strokeen
dc.subjectNeuronalen
dc.subjectPlasmaen
dc.subject.meshAcute Disease
dc.subject.meshAged
dc.subject.meshAged, 80 and over
dc.subject.meshAnimals
dc.subject.meshBrain
dc.subject.meshBrain Ischemia
dc.subject.meshCells, Cultured
dc.subject.meshCoculture Techniques
dc.subject.meshDisease Models, Animal
dc.subject.meshDisease Progression
dc.subject.meshEndothelial Cells
dc.subject.meshFemale
dc.subject.meshHumans
dc.subject.meshInfarction, Middle Cerebral Artery
dc.subject.meshLeukemia Inhibitory Factor
dc.subject.meshMale
dc.subject.meshMiddle Aged
dc.subject.meshNeuroglia
dc.subject.meshNeurons
dc.subject.meshRats
dc.subject.meshRats, Sprague-Dawley
dc.subject.meshStroke
dc.subject.meshUp-Regulation
dc.titleLeukaemia inhibitory factor is over-expressed by ischaemic brain tissue concomitant with reduced plasma expression following acute stroke.en
dc.typeArticleen
dc.contributor.departmentThe Department of Biology, Chemistry and Health Science, Manchester Metropolitan University, Manchester, UK. m.a.slevin@mmu.ac.uken
dc.identifier.journalEuropean Journal of Neurologyen
html.description.abstractLeukaemia inhibitory factor (LIF) is a glycoprotein of the interleukin-6 family, which has potent pro-inflammatory properties and is involved in regulation of neuronal differentiation. We have previously identified its upregulation in gene microarrays following acute ischaemic stroke in man. LIF expression and localization was measured in human ischaemic stroke autopsy specimens, in a rat model of middle cerebral artery occlusion (MCAO) and in human foetal neural cell cultures following oxygen-glucose deprivation (OGD) by Western blotting and immunohistochemistry. Circulating LIF was determined in the plasma of patients in the hyper-acute stroke phase using a multiplex enzyme-linked-immunosorbent serologic assay system. Patients demonstrated an increase in LIF expression in peri-infarcted regions with localization in neurons and endothelial cells of microvessels surrounding the infarcted core. The rat MCAO model showed similar upregulation in neurons with a peak increase at 90 min. Circulating serum LIF expression was significantly decreased in the hyper-acute phase of stroke. Brain-derived neurons and glia cultured in vitro demonstrated an increase in gene/protein and protein expression respectively following exposure to OGD. Increased LIF expression in peri-infarcted regions and sequestration from the peripheral circulation in acute stroke patients are characteristic of the pathobiological response to ischaemia and tissue damage.


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