Shen Zhida, Chen Qi, Ying Hangying, Ma Zetao, Bi Xukun, Li Xiaoting, Wang Meihui, Jin Chongying, Lai Dongwu, Zhao Yanbo, Fu Guosheng
Department of Cardiology, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310016, P.R. China.
Biomedical Research Center, Sir Run Run Shaw Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang 310016, P.R. China.
Exp Ther Med. 2020 Jan;19(1):499-510. doi: 10.3892/etm.2019.8239. Epub 2019 Nov 22.
Type 2 diabetes mellitus (DM) is a metabolic disease with worldwide prevalence that is associated with a decrease in the number and function of endothelial progenitor cells (EPCs). The aim of the present study was to explore the potential hub genes of EPCs in patients with type 2 DM. Differentially expressed genes (DEGs) were screened from a public microarray dataset (accession no. GSE43950). Pathway and functional enrichment analyses were performed using the Database for Annotation, Visualization and Integrated Discovery. The protein-protein interaction (PPI) network was visualized. The most significantly clustered modules and hub genes were identified using Cytoscape. Furthermore, hub genes were validated by quantitative PCR analysis of EPCs isolated from diabetic and normal subjects. Subsequently, weighted gene co-expression network analysis (WGCNA) was performed to identify the modules incorporating the genes exhibiting the most significant variance. A total of 970 DEGs were obtained and they were mainly accumulated in inflammation-associated pathways. A total of 9 hub genes were extracted from the PPI network and the highest differential expression was determined for the interleukin 8 (IL8) and CXC chemokine ligand 1 (CXCL1) genes. In the WGCNA performed to determine the modules associated with type 2 DM, one module incorporated IL8 and CXCL1. Finally, pathway enrichment of 10% genes in the pink module ordered by intramodular connectivity (IC) was associated with the IL17 and the chemokine signaling pathways. The present results revealed that the expression of IL8 and CXCL1 may serve important roles in the pathophysiology of EPCs during type 2 DM and inflammatory response may be critical for the reduced number and hypofunction of EPCs isolated from patients with diabetes.
2型糖尿病(DM)是一种全球流行的代谢性疾病,与内皮祖细胞(EPCs)数量和功能的减少有关。本研究的目的是探索2型糖尿病患者EPCs的潜在关键基因。从公共微阵列数据集(登录号GSE43950)中筛选差异表达基因(DEGs)。使用注释、可视化和综合发现数据库进行通路和功能富集分析。对蛋白质-蛋白质相互作用(PPI)网络进行可视化。使用Cytoscape识别最显著聚类的模块和关键基因。此外,通过对从糖尿病和正常受试者分离的EPCs进行定量PCR分析来验证关键基因。随后,进行加权基因共表达网络分析(WGCNA)以识别包含表现出最显著差异的基因的模块。共获得970个DEGs,它们主要聚集在炎症相关通路中。从PPI网络中提取了9个关键基因,确定白细胞介素8(IL8)和CXC趋化因子配体1(CXCL1)基因的差异表达最高。在用于确定与2型糖尿病相关模块的WGCNA中,一个模块包含IL8和CXCL1。最后,按模块内连通性(IC)排序的粉色模块中10%基因的通路富集与IL17和趋化因子信号通路相关。目前的结果表明,IL8和CXCL1的表达可能在2型糖尿病期间EPCs的病理生理学中起重要作用,炎症反应可能对从糖尿病患者分离的EPCs数量减少和功能低下至关重要。