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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

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

  • 影响因子:2.75
  • DOI:10.1007/s12192-020-01070-8
  • 作者列表:"Huang, Pan","Tang, Weihong","Shen, Rong","Ju, Xiaoli","Shao, Genbao","Xu, Xiao","Jiang, Anqi","Qian, Xiaobin","Chen, Miao","Zhou, Zhengrong","Ren, Caifang
  • 发表时间:2020-02-22
Abstract

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.

摘要

应激性胃溃疡是创伤后影响患者的常见并发症之一,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) 、和大鼠胃溃疡恢复 3 天 (T3),并进行生物信息学分析,以确定基因表达和生物通路的变化。通过 STRING 构建差异表达基因 (DEGs) 的蛋白质-蛋白质相互作用 (PPI) 网络,并通过 Cytoscape 软件进行可视化。还构建了 hub DEGs 的相关转录因子 (TFs)-基因调控网络。两两比较分别获得 103 (T0_C) 、 127 (T3_T0) 和 13 (T3_C) 个 DEGs。基因本体 (Gene ontology,GO) 富集分析表明,T0_C 和 T3_T0 中的 DEGs 在响应含氧化合物、响应有机物和响应外界刺激时显著富集。通路分析提示 DEGs 在 TNF 信号通路、 PPAR 信号通路、细胞凋亡和 IL-17 信号通路中富集。从 T0_C 和 T3_T0 的 PPI 网络中获得了 7 个枢纽基因 (Fos,6月,Nfkbia,Dusp1,Pim3,Junb 和 Fosb)。具有密切交互的关键 TFs,如 Fos,6月,Nfkbia,Junb,Egr1 和 Fosb, 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,有助于揭示胃溃疡发生和修复的分子机制,并为人类胃溃疡的治疗提供参考。

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