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Analysis of candidate biomarkers and related transcription factors involved in the development and restoration of stress-induced gastric ulcer by transcriptomics.
Cell Stress and Chaperones ( IF 3.3 ) Pub Date : 2020-02-22 , DOI: 10.1007/s12192-020-01070-8
Pan Huang 1 , Weihong Tang 1 , Rong Shen 1 , Xiaoli Ju 1 , Genbao Shao 1 , Xiao Xu 1 , Anqi Jiang 1 , Xiaobin Qian 1 , Miao Chen 1 , Zhengrong Zhou 1 , Caifang Ren 1
Affiliation  

Stress-induced gastric ulcer is one of the common complications affecting patients after trauma, mainly leading to gastrointestinal bleeding and perforation, and severe cases may be life-threatening. However, the molecular mechanism of stress-induced gastric ulcer remains unclear. In the present study, RNA-sequencing was performed on gastric tissues of normal rats (C), stress-induced gastric ulcer rats (T0), and rats recovered from gastric ulcer for 3 days (T3), and bioinformatics analysis was performed to determine changes in gene expression and biological pathways. The protein–protein interaction (PPI) networks of differentially expressed genes (DEGs) were constructed by STRING and visualized by the Cytoscape software. The associated transcriptional factor (TFs)–gene regulatory network of the hub DEGs was also constructed. Pairwise comparisons obtained 103 (T0_C), 127 (T3_T0), and 13 (T3_C) DEGs, respectively. Gene ontology (GO) enrichment analysis indicated DEGs in T0_C and T3_T0 were significantly enriched in response to oxygen-containing compound, response to organic substance, and response to external stimulus. Pathway analysis suggested that DEGs were enriched in TNF signaling pathway, PPAR signaling pathway, apoptosis, and IL-17 signaling pathway. Seven hub genes (Fos, Jun, Nfkbia, Dusp1, Pim3, Junb, and Fosb) were obtained from the PPI networks of T0_C and T3_T0. Key TFs with close interactions, such as Fos, Jun, Nfkbia, Junb, Egr1, and Fosb, were screened This study used RNA-sequencing and bioinformatics analysis to screen out genes associated with gastric ulcer, which can help reveal the molecular mechanism of gastric ulcer development and restoration, and provide reference for the treatment of human gastric ulcers.

中文翻译:


通过转录组学分析参与应激性胃溃疡发生和恢复的候选生物标志物和相关转录因子。



应激性胃溃疡是创伤后患者常见的并发症之一,主要导致消化道出血和穿孔,严重者可能危及生命。然而,应激性胃溃疡的分子机制仍不清楚。本研究对正常大鼠(C)、应激性胃溃疡大鼠(T0)和胃溃疡恢复3天大鼠(T3)的胃组织进行RNA测序,并进行生物信息学分析以确定基因表达和生物学途径的变化。差异表达基因(DEG)的蛋白质-蛋白质相互作用(PPI)网络通过STRING构建并通过Cytoscape软件可视化。还构建了中心DEG的相关转录因子(TF)-基因调控网络。两两比较分别获得 103 (T0_C)、127 (T3_T0) 和 13 (T3_C) DEG。基因本体(GO)富集分析表明,T0_C和T3_T0中的DEG对含氧化合物的响应、对有机物质的响应以及对外部刺激的响应显着富集。通路分析表明DEGs富集于TNF信号通路、PPAR信号通路、细胞凋亡和IL-17信号通路。从 T0_C 和 T3_T0 的 PPI 网络中获得了 7 个枢纽基因(Fos、Jun、Nfkbia、Dusp1、Pim3、Junb 和 Fosb)。筛选了Fos、Jun、Nfkbia、Junb、Egr1、Fosb等相互作用密切的关键转录因子本研究通过RNA测序和生物信息学分析筛选出与胃溃疡相关的基因,有助于揭示胃溃疡的分子机制溃疡的发生和恢复,为人类胃溃疡的治疗提供参考。
更新日期:2020-02-22
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