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The class B scavenger receptor CD36 mediates free radical production and tissue injury in cerebral ischemia

Title
The class B scavenger receptor CD36 mediates free radical production and tissue injury in cerebral ischemia
Authors
Cho S.Park E.-M.Febbraio M.Anrather J.Park L.Racchumi G.Silverstein R.L.Iadecola C.
Ewha Authors
박은미
SCOPUS Author ID
박은미scopus
Issue Date
2005
Journal Title
Journal of Neuroscience
ISSN
0270-6474JCR Link
Citation
vol. 25, no. 10, pp. 2504 - 2512
Indexed
SCI; SCIE; SCOPUS scopus
Abstract
The class B scavenger receptor CD36 is involved in the cytotoxicity associated with inflammation, but its role in the inflammatory reaction that accompanies cerebral ischemia has not been examined. In this study, we investigated whether CD36 contributes to the brain damage produced by cerebral ischemia. The middle cerebral artery was transiently occluded in wild-type mice and in mice deficient in CD36. In wild-type mice, CD36 protein expression was increased in the ischemic brain, such that it was located predominantly in cells expressing the microglia/macrophage marker CD11b. The infarct produced by middle cerebral artery occlusion was 49% smaller in CD36-null mice than in wild-type controls, an effect associated with improved neurological function. The attenuation in brain injury in CD36 nulls could not be attributed to differences in cerebral blood flow during ischemia-reperfusion. However, the increase in reactive oxygen species (ROS) produced by cerebral ischemia was markedly attenuated in CD36-null mice in the early stage after reperfusion. The data unveil a previously unrecognized role of CD36 in ischemia-induced ROS production and brain injury. Modulation of CD36 signaling may provide a new strategy for the treatment of ischemic stroke. Copyright © 2005 Society for Neuroscience.
DOI
10.1523/JNEUROSCI.0035-05.2005
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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