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坐骨神经损伤后大鼠背根神经节的基因表达谱变化

Gene expression profile changes in rat dorsal horn after sciatic nerve injury.

作者信息

Wang Jing, Ma Song-He, Tao Rong, Xia Ling-Jie, Liu Lin, Jiang Ying-Hai

机构信息

a Department of Pain Management , Henan Provincial People's Hospital, The People's Hospital of Zhengzhou University , Zhengzhou , China.

出版信息

Neurol Res. 2017 Feb;39(2):176-182. doi: 10.1080/01616412.2016.1273590. Epub 2016 Dec 30.

Abstract

OBJECTIVE

This study aims to investigate gene expression changes in rat dorsal horns after sciatic nerve injury (SNI).

METHODS

The GSE18803 microarray data collected from young and adult rats were downloaded from GEO. After preprocessing, differentially expressed genes (DEGs) between SNI and sham-operated groups were selected using Limma package, in young and adult group, respectively, followed by Venn analysis. Then, enrichment analyses were performed for these DEGs using DAVID. The STRING database was used to identify protein-protein interactions (PPIs) among these DEGs, and the module network was further extracted using plugin ClusterONE. Finally, protein domain enrichment analysis of DEGs in each module was performed using InterPro database.

RESULTS

Totally, 210 and 50 DEGs were identified in adult and young group, respectively. Among them, 160 were specific in adult group (e.g. CCL2, NF-κB1 and RAC2); 9 were specific in young group (e.g. ILF3 and LYVE1); and 41 were common in both two groups (e.g. FCER1G, C1QA, C1QB and C1QC). The up-regulated DEGs were mostly enriched in immune response-related biological processes, as well as 15 immune- and inflammation-related pathways. Then, two modules were identified in PPI network. CCL2 and NF-κB1 had high connectivity degrees in module 1, and RAC2, FCER1G and CD68 in module 2.

CONCLUSION

CCL2, NF-κB1, RAC2, FCER1G and C1Q may contribute to the generation of neuropathic pain after SNI via immune and defense pathways. Among the five genes, the first three are specific in adult population, while the latter two are age-independent. They all might function through involvement of these immune or inflammatory pathways.

摘要

目的

本研究旨在调查坐骨神经损伤(SNI)后大鼠背根神经节中的基因表达变化。

方法

从GEO下载从幼年和成年大鼠收集的GSE18803微阵列数据。预处理后,分别在幼年和成年组中使用Limma软件包选择SNI组和假手术组之间的差异表达基因(DEG),随后进行Venn分析。然后,使用DAVID对这些DEG进行富集分析。使用STRING数据库识别这些DEG之间的蛋白质-蛋白质相互作用(PPI),并使用插件ClusterONE进一步提取模块网络。最后,使用InterPro数据库对每个模块中的DEG进行蛋白质结构域富集分析。

结果

成年组和幼年组分别共鉴定出210个和50个DEG。其中,160个在成年组中具有特异性(例如CCL2、NF-κB1和RAC2);9个在幼年组中具有特异性(例如ILF3和LYVE1);41个在两组中都常见(例如FCER1G、C1QA、C1QB和C1QC)。上调的DEG大多富集于免疫反应相关的生物学过程以及15条免疫和炎症相关途径。然后,在PPI网络中鉴定出两个模块。CCL2和NF-κB1在模块1中具有较高的连接度,而RAC2、FCER1G和CD68在模块2中具有较高的连接度。

结论

CCL2、NF-κB1、RAC2、FCER1G和C1Q可能通过免疫和防御途径促成SNI后神经性疼痛的产生。在这五个基因中,前三个在成年群体中具有特异性,而后两个与年龄无关。它们可能都通过参与这些免疫或炎症途径发挥作用。

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