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首页> 外文期刊>Journal of stroke and cerebrovascular diseases: The official journal of National Stroke Association >Global Transcriptomic Profiling of Cortex and Striatum: Cerebral Injury after Ischemia/Reperfusion in a Mouse Model
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Global Transcriptomic Profiling of Cortex and Striatum: Cerebral Injury after Ischemia/Reperfusion in a Mouse Model

机译：皮质和纹状体的全局转录组分析：脑损伤在小鼠模型中缺血/再灌注后

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Objective: This study aims to investigate the molecular mechanism of injury development in the cortex and the striatum after cerebral ischemia/reperfusion (I/R). Methods: Gene expression data (GSE23160) in the cortex and the striatum of an intraluminal middle cerebral artery occlusion-I/R mouse model (N = 12) and sham controls (N = 4) were downloaded from the Gene Expression Omnibus. Limma package was used to identify the differentially expressed genes (DEGs) between the I/R (2, 8, and 24 hours) and control groups. Correlation analysis was then performed to identify the highly correlated differentially expressed genes (HCDEGs). STRING and Cytoscape software were used to construct a protein-protein interaction (PPI) network of HCDEGs. Furthermore, Venny 2.0 was used to identify common overlapped DEGs whose transcription factors (TFs) were predicted using iRegulon in Cytoscape. Results: For the cortex and the striatum, 2295 and 2282 DEGs were respectively identified between the I/R group and the controls, and were classified into 3 and 2 correlation modules. For each module, a PPI network was constructed, and Toll-like receptor 2 (Tlr2, degree = 25), interleukin 1 beta (Il1b, degree = 21), and heme oxygenase-1 (Hmox1, degree = 17) had high connective degrees. Furthermore, 29 common overlapped DEGs were found across time and tissue, which might be targeted by 13 TFs. Especially, Tlr2, Il1b, and Hmox1 were targeted by myeloblastosis protein (Myb, target count = 16) and FBJ osteosarcoma protein (Fos, target count = 15). Moreover, plasminogen activator urokinase receptor (Plaur) was targeted by Fos, and it was an HCDEG in correlation modules of both cortex and striatum. Upregulation of Tlr2, Il1b, Hmox1, and Plaur in I/R injury was confirmed using quantitative polymerase chain reaction and immunohistochemical staining. Conclusion: Tlr2, Il1b, Hmox1, and Plaur regulated by Myb and Fos might participate in cortex and striatum injury after cerebral I/R.
机译：目的：本研究旨在探讨脑缺血/再灌注（I / R）后皮质损伤和纹状体损伤的分子机制。方法：从基因表达综合症下载基因表达数据（GSE23160）中的皮层中的基因表达数据（GSE23160）和腔内中间脑动脉闭塞-1 / R小鼠模型（n = 12）和假对照（n = 4）。利用LiMMA包来鉴定I / R（2,8和24小时）和对照组之间的差异表达基因（DEGS）。然后进行相关分析以鉴定高度相关的差异表达基因（HCDEG）。字符串和细胞展软件用于构建HCDEG的蛋白质 - 蛋白质相互作用（PPI）网络。此外，venny 2.0用于鉴定使用Iregulon在Cytoscape中预测其转录因子（TFS）的共同重叠的eg。结果：对于皮质，纹状体，2295和2282℃分别鉴定在I / R组和对照之间，并被分为3和2个相关模块。对于每个模块，构建了PPI网络，并且可以接受达到的受体2（TLR2，度= 25），白细胞介素1β（IL1B，度= 21）和血红素氧合酶-1（HMOX1，度= 17）具有高结缔组织程度。此外，在时间和组织中发现了29个常见的重叠的次数，其可能由13个TF靶向。特别是，TLR2，IL1B和HMOX1由髓母细胞分子蛋白（MYB，靶计数= 16）和FBJ骨肉瘤蛋白（FOS，靶计数= 15）靶向。此外，纤溶酶原激活剂尿激酶受体（猪）由FOS靶向，并且是皮质和纹状体的相关模块中的HCDEG。使用定量聚合酶链式反应和免疫组化染色来确认I / R损伤中TLR2，IL1B，HMOX1和血脂的上调。结论：TLR2，IL1B，HMOX1和MYB和FOS调节的PRAUR可能会参与脑I / R后皮质和纹状体损伤。

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