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Brain Advance Access originally published online on April 24, 2006
Brain 2006 129(6):1426-1437; doi:10.1093/brain/awl094
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© The Author (2006). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Increased thalamic neurodegeneration following ischaemic cortical stroke in osteopontin-deficient mice

Michael Schroeter1, Philipp Zickler1, David T. Denhardt2, Hans-Peter Hartung1 and Sebastian Jander1

1 Department of Neurology, Heinrich Heine University Düsseldorf, Germany 2 Department of Cell Biology and Neuroscience, Rutgers University Piscataway, NJ 08854-8082, USA

Correspondence to: Dr Sebastian Jander, Department of Neurology, Heinrich Heine University, Moorenstr. 5, D-40225 Düsseldorf, Germany E-mail: jander{at}uni-duesseldorf.de

Inflammation aggravates brain injury caused by stroke and neurodegeneration. Osteopontin (OPN) is a cytokine-like glycoprotein that binds to various integrins and CD44 variants. OPN exerts proinflammatory effects in autoimmune conditions but also has cytoprotective properties and participates in wound healing. In this study, we addressed the role of OPN in ischaemic brain injury using OPN knock-out (KO) mice in models of cortical stroke. Compared with wild-type animals, OPN KO mice exhibited unaltered infarct development at the primary injury site but greatly increased retrograde degeneration of the ipsilateral thalamus. Thalamic neurodegeneration in OPN-deficient mice was associated with pronounced microglia activation and inflammatory gene expression and could be attenuated via pharmacological blockade of the inducible nitric oxide synthase (iNOS). Therefore, delayed neurodegeneration in OPN-deficient mice was at least partly due to an excessive release of nitric oxide via the iNOS pathway. Neuroprotective and anti-inflammatory effects of OPN may be relevant for a variety of neurological disease conditions.

Key Words: ischaemic stroke; inflammation; neurodegeneration; nitric oxide; microglia

Abbreviations: iNOS, inducible nitric oxide synthase; MCAO, middle cerebral artery occlusion; OPN, osteopontin; PCR, polymerase chain reaction; WT, wild-type

Received January 12, 2006. Revised March 15, 2006. Accepted March 22, 2006.


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