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基于生物信息学的方法预测 MIR-17-5P 通过调节 ABCA1 和 CD69 参与季节性变应性鼻炎的发病机制。

Bioinformatics-Based Approaches Predict That MIR-17-5P Functions in the Pathogenesis of Seasonal Allergic Rhinitis Through Regulating ABCA1 and CD69.

机构信息

1 ENT Department, Inner Mongolia People's Hospital, Hohhot, China.

2 Clinical Medical Research Center, Inner Mongolia People's Hospital, Hohhot, China.

出版信息

Am J Rhinol Allergy. 2019 May;33(3):269-276. doi: 10.1177/1945892418823388. Epub 2019 Jan 8.

DOI:10.1177/1945892418823388
PMID:30616374
Abstract

OBJECTIVE

As the most prevalent type of rhinitis, allergic rhinitis is consisted of seasonal allergic rhinitis (SAR) and perennial allergic rhinitis. This study is carried out for revealing the mechanisms of SAR.

METHODS

Microarray data set GSE43523 (including 7 SAR nasal epithelial cells and 5 nonallergic control nasal epithelial cells) was extracted from Gene Expression Omnibus database. Based on limma package, differential expression analysis for the 2 groups was performed to obtain differentially expressed genes (DEGs). Using Multifaceted Analysis Tool for Human Transcriptome online tool, the functions involving the DEGs were predicted by enrichment analysis. Combined with Cytoscape software, protein-protein interaction (PPI) network was built and a significant network module was acquired. In addition, transcription factor (TF)-target and miRNA-target pairs were predicted using WebGestalt tool, and then TF-miRNA-target regulatory network was built by Cytoscape software.

RESULTS

There were 274 DEGs between rhinitis and control samples, including 144 upregulated genes and 130 downregulated genes. After PPI for the DEGs was built, a significant network module was identified. In the TF-miRNA-target regulatory network, ABCA1, CPEB4, CD69, MIR-17-5P, and CREB had higher degrees. Furthermore, both ABCA1 and CD69 were targeted by MIR-17-5P in the regulatory network.

CONCLUSION

CPEB4 and CREB might be implicated in the pathogenesis of SAR. Besides, MIR-17-5P might also act in SAR via targeting ABCA1 and CD69.

摘要

目的

变应性鼻炎是最常见的鼻炎类型,包括季节性变应性鼻炎(SAR)和常年性变应性鼻炎。本研究旨在揭示 SAR 的发病机制。

方法

从基因表达综合数据库中提取 GSE43523 芯片数据集(包括 7 例 SAR 鼻上皮细胞和 5 例非变应性对照鼻上皮细胞)。基于 limma 包,对 2 组进行差异表达分析,获得差异表达基因(DEGs)。利用 Multifaceted Analysis Tool for Human Transcriptome 在线工具进行富集分析,预测涉及 DEGs 的功能。结合 Cytoscape 软件,构建蛋白质-蛋白质相互作用(PPI)网络,并获取显著网络模块。此外,使用 WebGestalt 工具预测转录因子(TF)-靶标和 miRNA-靶标对,然后通过 Cytoscape 软件构建 TF-miRNA-靶标调控网络。

结果

在 SAR 组和对照组样本之间有 274 个 DEGs,包括 144 个上调基因和 130 个下调基因。构建 DEGs 的 PPI 后,确定了一个显著的网络模块。在 TF-miRNA-靶标调控网络中,ABCA1、CPEB4、CD69、MIR-17-5P 和 CREB 的度数较高。此外,MIR-17-5P 在调控网络中同时靶向 ABCA1 和 CD69。

结论

CPEB4 和 CREB 可能参与 SAR 的发病机制。此外,MIR-17-5P 可能通过靶向 ABCA1 和 CD69 参与 SAR 的发病机制。

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