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Brain Advance Access published online on April 24, 2006
Brain, 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
Received January 12, 2006
Revised March 15, 2006
Accepted March 22, 2006

Article

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

Michael Schroeter 1, Philipp Zickler 1, David T. Denhardt 2, Hans-Peter Hartung 1, and Sebastian Jander 1 *

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

* To whom correspondence should be addressed.
Sebastian Jander, E-mail: jander{at}uni-duesseldorf.de


  Abstract

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.

Keywords: ischaemic stroke; inflammation; neurodegeneration; nitric oxide; microglia.
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