Department of Functional Anatomy, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
Department of Orthopaedic Surgery, Graduate School of Medicine, Chiba University, 1-8-1 Inohana, Chuo-ku, Chiba, 260-8670, Japan.
Mol Brain. 2020 Apr 7;13(1):57. doi: 10.1186/s13041-020-00598-1.
The neuroinflammation in the ischemic brain could occur as sterile inflammation in response to damage-associated molecular patterns (DAMPs). However, its long-term dynamic transcriptional changes remain poorly understood. It is also unknown whether this neuroinflammation contributes to the recovery or just deteriorates the outcome. The purpose of this study is to characterize the temporal transcriptional changes in the post-stroke brain focusing on DAMPs-related genes by RNA-sequencing during the period of 28 days. We conducted the RNA-sequencing on day 1, 3, 7, 14, 28 post-stroke in the mouse photothrombosis model. The gross morphological observation showed the ischemic lesion on the ipsilateral cortex turned into a scar with the clearance of cellular debris by day 28. The transcriptome analyses indicated that post-stroke period of 28 days was classified into four categories (I Baseline, II Acute, III Sub-acute-#1, IV Sub-acute-#2 phase). During this period, the well-known genes for DAMPs, receptors, downstream cascades, pro-inflammatory cytokines, and phagocytosis were transcriptionally increased. The gene ontology (GO) analysis of biological process indicated that differentially expressed genes (DEGs) are genetically programmed to achieve immune and inflammatory pathways. Interestingly, we found the biphasic induction of various genes, including DAMPs and pro-inflammatory factors, peaking at acute and sub-acute phases. At the sub-acute phase, we also observed the induction of genes for phagocytosis as well as regulatory and growth factors. Further, we found the activation of CREB (cAMP-response element binding protein), one of the key players for neuronal plasticity, in peri-ischemic neurons by immunohistochemistry at this phase. Taken together, these findings raise the possibility the recurrent inflammation occurs at the sub-acute phase in the post-stroke brain, which could be involved in the debris clearance as well as neural reorganization.
脑缺血后的神经炎症可能是对损伤相关分子模式 (DAMPs) 的无菌性炎症反应。然而,其长期的动态转录变化仍知之甚少。也不知道这种神经炎症是有助于恢复还是只会使结果恶化。本研究的目的是通过 RNA 测序来描述中风后大脑中与 DAMPs 相关的基因的时间转录变化,研究时间跨度为 28 天。我们在光血栓模型中风后第 1、3、7、14 和 28 天进行了 RNA 测序。大体形态观察显示,同侧皮质的缺血性损伤在第 28 天变成了疤痕,细胞碎片被清除。转录组分析表明,中风后 28 天的时期可分为四类 (I 基线、II 急性期、III 亚急性期 #1、IV 亚急性期 #2)。在此期间,DAMPs、受体、下游级联、促炎细胞因子和吞噬作用的众所周知的基因转录水平增加。生物学过程的基因本体 (GO) 分析表明,差异表达基因 (DEGs) 是按照遗传程序来实现免疫和炎症途径的。有趣的是,我们发现各种基因(包括 DAMPs 和促炎因子)呈双相诱导,在急性期和亚急性期达到高峰。在亚急性期,我们还观察到吞噬作用以及调节和生长因子的基因诱导。此外,我们通过免疫组织化学在该阶段发现,CREB(cAMP 反应元件结合蛋白)被激活,CREB 是神经元可塑性的关键参与者之一。综上所述,这些发现表明中风后大脑中的亚急性期可能会反复发生炎症,这可能涉及碎片清除和神经重组。