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首页> 外文期刊>Journal of Neurochemistry: Offical Journal of the International Society for Neurochemistry >Lack of the scavenger receptor CD36 alters microglial phenotypes after neonatal stroke
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Lack of the scavenger receptor CD36 alters microglial phenotypes after neonatal stroke

机译：新生儿中风后缺乏清道夫受体CD36改变小胶质细胞表型。

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摘要

The stage of brain development at the time of stroke has a major impact on the pathophysiological mechanisms of ischemic damage, including the neuroinflammatory response. Microglial cells have been shown to contribute to acute and subchronic injury in adult stroke models, whereas in neonatal rodents we showed that microglial cells serve as endogenous neuroprotectants early following transient middle cerebral artery occlusion, limiting neuroinflammation and injury. In the neonate, microglial depletion or lack of the scavenger receptor CD36 exacerbates injury. In this study we asked if lack of CD36 affects microglial phenotypes after neonatal stroke. Using RT-PCR we characterized the patterns of gene expression in microglia isolated from injured regions following acute transient middle cerebral artery occlusion in postnatal day 10 mice and showed that expression of several pro-inflammatory genes, including Toll-like receptors, remains largely unaffected in activated microglia in injured regions. Using multiple biochemical assays we demonstrated that lack of CD36 alters several functions of microglia in acutely injured neonatal brain: it further enhances accumulation of the chemokine MCP-1, affects the number of CD11b(+)/CD45(+) cells, along with protein expression of its co-receptor, Toll-like receptor 2, but does not affect accumulation of superoxide in microglia or the cytokines TNF and IL-1 in injured regions.
机译：中风时大脑发育的阶段对缺血性损伤的病理生理机制（包括神经炎性反应）有重要影响。在成年卒中模型中，小胶质细胞已被证明可导致急性和亚慢性损伤，而在新生啮齿类动物中，我们显示小胶质细胞在短暂性大脑中动脉闭塞后可作为内源性神经保护剂，从而限制了神经炎症和损伤。在新生儿中，小胶质细胞的耗竭或清除剂受体CD36的缺乏加剧了损伤。在这项研究中，我们询问缺乏CD36是否会影响新生儿卒中后的小胶质细胞表型。使用RT-PCR，我们表征了出生后第10天小鼠急性短暂性中脑动脉闭塞后从受损区域分离的小胶质细胞中的基因表达模式，并显示了包括Toll样受体在内的几种促炎基因的表达在很大程度上未受影响。在受伤区域激活小胶质细胞。使用多种生化分析，我们证明了CD36的缺乏改变了急性受损新生儿脑中小胶质细胞的几种功能：它进一步增强了趋化因子MCP-1的积累，影响CD11b（+）/ CD45（+）细胞以及蛋白质的数量其共同受体Toll样受体2的表达，但不影响小胶质细胞中超氧化物的积累或受损区域的细胞因子TNF和IL-1的表达。

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