The class B scavenger receptor CD36 mediates free radical production and tissue injury in cerebral ischemia. J Neurosci 2005 Mar 09;25(10):2504-12
Date
03/11/2005Pubmed ID
15758158Pubmed Central ID
PMC6725161DOI
10.1523/JNEUROSCI.0035-05.2005Scopus ID
2-s2.0-14944379101 (requires institutional sign-in at Scopus site) 186 CitationsAbstract
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.
Author List
Cho S, Park EM, Febbraio M, Anrather J, Park L, Racchumi G, Silverstein RL, Iadecola CAuthor
Roy L. Silverstein MD Professor in the Medicine department at Medical College of WisconsinMESH terms used to index this publication - Major topics in bold
AnimalsBrain Ischemia
CD36 Antigens
Free Radicals
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Reactive Oxygen Species
Reperfusion Injury
