The class B scavenger receptor CD36 mediates free radical production and tissue injury in cerebral ischemia
The class B scavenger receptor CD36 mediates free radical production and tissue injury in cerebral ischemia
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DOI：
10.1523/jneurosci.0035-05.2005
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发表时间：
2005-03-09
影响因子：
5.3
通讯作者：
Iadecola, C
中科院分区：
文献类型：
--
作者：
Cho, S;Park, EM;Iadecola, C
B类清道夫受体CD36参与与炎症相关的细胞毒性，但其在伴随脑缺血的炎症反应中的作用尚未得到研究。在这项研究中，我们研究了 CD36 是否会导致脑缺血引起的脑损伤。野生型小鼠和 CD36 缺陷小鼠的大脑中动脉被短暂闭塞。在野生型小鼠中，缺血性脑中 CD36 蛋白表达增加，因此它主要位于表达小胶质细胞/巨噬细胞标记物 CD11b 的细胞中。 CD36 缺失小鼠中大脑中动脉闭塞引起的梗塞比野生型对照小鼠小 49%，这种效应与神经功能的改善有关。 CD36 缺失中脑损伤的减弱不能归因于缺血再灌注期间脑血流量的差异。然而，CD36缺失小鼠在再灌注后的早期阶段，脑缺血产生的活性氧（ROS）的增加明显减弱。这些数据揭示了 CD36 在缺血诱导的 ROS 产生和脑损伤中的先前未被认识的作用。 CD36信号传导的调节可能为治疗缺血性中风提供新策略。
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.