Data_Sheet_1_Tandem Mass Tag-Based Quantitative Proteomic Analysis Reveals Pathways Involved in Brain Injury Induced by Chest Exposure to Shock Waves.PDF

Recurrent chest blast exposure can lead to brain inflammation, oxidative stress, and mental disorders in soldiers. However, the mechanism that underlies brain injury caused indirectly by chest blasts remains unclear. It is urgent to find additional reliable biomarkers to reveal the intimate details of the pathogenesis of this phenomenon. We used the term tandem mass tag (TMT) labeling combined with liquid chromatography–tandem mass spectrometry (LC-MS/MS) to screen for differentially expressed proteins in rat brain at different time points after a chest blast. Data are available via ProteomeXchange with the identifier PXD025204. Gene Ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG), the Database for Annotation, Visualization and Integrated Discovery (DAVID), and Cytoscape analyses were used to analyze the proteomic profiles of blast-exposed rats. In addition, we performed Western blotting to verify protein levels. We identified 6,931 proteins, of which 255 were differentially expressed and 43, 84, 52, 97, and 49 were identified in brain tissues at 12, 24, 48, and 72 h and 1 week after chest blast exposure, respectively. In this study, the GO, KEGG, Clusters of Orthologous Groups of proteins, and Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) analyses indicated that brain damage caused by chest blast exposure involved many important biological processes and signaling pathways, such as inflammation, cell adhesion, phagocytosis, neuronal and synaptic damage, oxidative stress, and apoptosis. Furthermore, Western blotting confirmed that these differentially expressed proteins and affected signaling pathways were associated with brain damage caused by chest blast exposure. This study identifies potential protein biomarkers of brain damage caused indirectly by chest blast and new targets for the treatment of this condition.

反复胸部爆炸暴露可导致士兵出现脑部炎症、氧化应激及精神障碍。然而，胸部爆炸间接引发脑损伤的具体分子机制仍未阐明。亟需发掘更多可靠的生物标志物，以深入解析该类脑损伤的发病机制全貌。本研究采用串联质量标签（tandem mass tag, TMT）标记结合液相色谱-串联质谱（liquid chromatography–tandem mass spectrometry, LC-MS/MS）技术，对胸部爆炸暴露后不同时间点的大鼠脑组织差异表达蛋白进行筛选。相关数据集可通过ProteomeXchange数据库获取，检索编号为PXD025204。本研究通过基因本体论（Gene Ontology, GO）、京都基因与基因组百科全书（Kyoto Encyclopedia of Genes and Genomes, KEGG）、注释、可视化与整合发现数据库（Database for Annotation, Visualization and Integrated Discovery, DAVID）及Cytoscape软件，对爆炸暴露大鼠的蛋白质组学特征进行分析。此外，本研究采用蛋白质免疫印迹（Western blotting）验证差异蛋白的表达水平。本研究共鉴定得到6931个蛋白质，其中255个为差异表达蛋白；在胸部爆炸暴露后12、24、48、72小时及1周的大鼠脑组织中，分别鉴定出43、84、52、97及49个差异表达蛋白。本研究通过GO、KEGG、直系同源蛋白簇（Clusters of Orthologous Groups of proteins, COG）及相互作用基因/蛋白质检索工具（Search Tool for the Retrieval of Interacting Genes/Proteins, STRING）分析发现，胸部爆炸暴露引发的脑损伤涉及诸多重要生物学过程与信号通路，包括炎症反应、细胞黏附、吞噬作用、神经元与突触损伤、氧化应激及细胞凋亡等。进一步的蛋白质免疫印迹实验证实，上述差异表达蛋白及受调控的信号通路与胸部爆炸暴露所致脑损伤密切相关。本研究筛选出胸部爆炸间接致脑损伤的潜在蛋白质生物标志物，并为该类损伤的治疗提供了全新靶点。