Stroke Laboratory, Neurology Service, Department of Clinical Neurosciences, University Hospital Centre and University of Lausanne, CH-1011, Lausanne, Switzerland.
Department of Fundamental Neurosciences, University of Lausanne, CH-1005, Lausanne, Switzerland.
Sci Rep. 2019 Jan 24;9(1):507. doi: 10.1038/s41598-018-36598-4.
After ischemic stroke, in the lesion core as well as in the ischemic penumbra, evolution of tissue damage and repair is strongly affected by neuroinflammatory events that involve activation of local specialized glial cells, release of inflammatory mediators, recruiting of systemic cells and vascular remodelling. To take advantage of this intricate response in the quest to devise new protective therapeutic strategies we need a better understanding of the territorial and temporal interplay between stroke-triggered inflammatory and cell death-inducing processes in both parenchymal and vascular brain cells. Our goal is to describe structural rearrangements and functional modifications occurring in glial and vascular cells early after an acute ischemic stroke. Low and high scale mapping of the glial activation on brain sections of mice subjected to 30 minutes middle cerebral artery occlusion (MCAO) was correlated with that of the neuronal cell death, with markers for microvascular changes and with markers for pro-inflammatory (IL-1β) and reparative (TGFβ1) cytokines. Our results illustrate a time-course of the neuroinflammatory response starting at early time-points (1 h) and up to one week after MCAO injury in mice, with an accurate spatial distribution of the observed phenomena.
缺血性中风后,在病变核心区和缺血半暗带区,组织损伤和修复的演变受到强烈的神经炎症事件的影响,这些事件涉及局部特化神经胶质细胞的激活、炎症介质的释放、全身细胞的募集和血管重塑。为了利用这种复杂的反应,寻求新的保护治疗策略,我们需要更好地了解中风触发的炎症和细胞死亡诱导过程在实质和血管脑细胞中的时空相互作用。我们的目标是描述急性缺血性中风后早期发生在神经胶质细胞和血管细胞中的结构重排和功能改变。对接受 30 分钟大脑中动脉闭塞(MCAO)的小鼠脑切片上的神经胶质细胞激活进行低和高尺度的映射,并与神经元细胞死亡、微血管变化标志物以及促炎(IL-1β)和修复(TGFβ1)细胞因子标志物进行了相关性分析。我们的结果说明了在小鼠的 MCAO 损伤后早期(1 小时)到一周的时间内,神经炎症反应的时间过程,观察到的现象具有精确的空间分布。