Lack of the scavenger receptor CD36 alters microglial phenotypes after neonatal stroke.

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 TNFα and IL-1β in injured regions.