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The Journal of Neuroscience, February 13, 2008, 28(7):1649-1658; doi:10.1523/JNEUROSCI.5205-07.2008

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Neurobiology of Disease
Nuclear Factor-B Activation and Postischemic Inflammation Are Suppressed in CD36-Null Mice after Middle Cerebral Artery Occlusion

Alexander Kunz, Takato Abe, Karin Hochrainer, Munehisa Shimamura, Josef Anrather, Gianfranco Racchumi, Ping Zhou, and Costantino Iadecola

Division of Neurobiology, Weill Cornell Medical College, New York, New York 10021

Correspondence should be addressed to Dr. Costantino Iadecola, Division of Neurobiology, Weill Cornell Medical College, 411 East 69th Street, KB-410, New York, NY 10021. Email: coi2001{at}med.cornell.edu

CD36, a class-B scavenger receptor involved in multiple functions, including inflammatory signaling, may also contribute to ischemic brain injury through yet unidentified mechanisms. We investigated whether CD36 participates in the molecular events underlying the inflammatory reaction that accompanies cerebral ischemia and may contribute to the tissue damage. We found that activation of nuclear factor-B, a transcription factor that coordinates postischemic gene expression, is attenuated in CD36-null mice subjected to middle cerebral artery occlusion. The infiltration of neutrophils and the glial reaction induced by cerebral ischemia were suppressed. Treatment with an inhibitor of inducible nitric oxide synthase, an enzyme that contributes to the tissue damage, reduced ischemic brain injury in wild-type mice, but not in CD36 nulls. In contrast to cerebral ischemia, the molecular and cellular inflammatory changes induced by intracerebroventricular injection of interleukin-1β were not attenuated in CD36-null mice. The findings unveil a novel role of CD36 in early molecular events leading to nuclear factor-B activation and postischemic inflammation. Inhibition of CD36 signaling may be a valuable therapeutic approach to counteract the deleterious effects of postischemic inflammation.

Key words: inflammation; Nox-2; COX-2; IL-1β; myeloperoxidase; iNOS

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Received Aug. 27, 2007; revised Dec. 28, 2007; accepted Dec. 29, 2007.

Correspondence should be addressed to Dr. Costantino Iadecola, Division of Neurobiology, Weill Cornell Medical College, 411 East 69th Street, KB-410, New York, NY 10021. Email: coi2001{at}med.cornell.edu

This article has been cited by other articles:

				S. Muhammad, W. Barakat, S. Stoyanov, S. Murikinati, H. Yang, K. J. Tracey, M. Bendszus, G. Rossetti, P. P. Nawroth, A. Bierhaus, et al. The HMGB1 Receptor RAGE Mediates Ischemic Brain Damage J. Neurosci., November 12, 2008; 28(46): 12023 - 12031. [Abstract] [Full Text] [PDF]

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