基于系统生物学方法的龋病生化途径及蛋白网络分析

Z. Mohamadi, Z. Khamverdi, Amir Taherkhani
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引用次数: 0

摘要

背景:蛀牙是一种多因素疾病,其病因涉及多种因素。目的:本研究旨在揭示TD的主要基因和分子机制。方法:分析基因表达综合数据库(Gene Expression Omnibus, GEO)中的数据集GSE1629,以揭示TD患者与正常牙齿患者的差异表达基因(differential Expression genes, DEGs)。构建了蛋白-蛋白相互作用网络,揭示了最重要的簇、枢纽基因、转录因子(TFs)和参与TFs调控的蛋白激酶。还发现了TD的信号通路和基因本体术语失调。结果:共检测出196个deg(假发现率1)。PTPRC、ITGB2、TYROBP、MMP9、CXCL8、CD44、CCL2、C1QB、C3和SPP1被认为是枢纽基因。此外,BPTF和MAPK1分别被证明是可能参与TD发病机制的最高的tf和蛋白激酶。结论:PTPRC、ITGB2、TYROBP、MMP9、CXCL8、CD44、CCL2、C1QB、C3、SPP1、BPTF和MAPK1可能是治疗TD的潜在标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Biochemical Pathway and Protein-Network Analysis of Dental Caries Based on Systems Biology Approaches
Background: Tooth decay (TD) is a multifactorial disorder, and several factors are involved in its etiology. Objective: The present study aimed to unravel the main genes and molecular mechanisms underlying TD. Methods: The dataset GSE1629 in the Gene Expression Omnibus (GEO) database was analyzed to uncover differentially expressed genes (DEGs) in patients with TD compared to patients with sound teeth. A protein-protein interaction network was built, and the most important clusters, hub genes, transcription factors (TFs), and protein kinases involved in the regulation of TFs were disclosed. Signaling pathways and Gene Ontology terms dysregulated in TD were also identified. Results: A total of 196 DEGs were determined (false discovery rate<0.001; |Log2 fold change|>1). PTPRC, ITGB2, TYROBP, MMP9, CXCL8, CD44, CCL2, C1QB, C3, and SPP1 were considered hub genes. Further, BPTF and MAPK1 were demonstrated to be the highest TFs and protein kinases likely involved in the pathogenesis of TD, respectively. Conclusion: PTPRC, ITGB2, TYROBP, MMP9, CXCL8, CD44, CCL2, C1QB, C3, SPP1, BPTF, and MAPK1 may be regarded as potential markers for the therapeutic purposes of TD.
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