Department of Cardiology, The Affiliated Hospital of Yangzhou University, Yangzhou University, Yangzhou, Jiangsu, China.
Department of Cardiology, Northern Jiangsu People's Hospital, Yangzhou University, Yangzhou, Jiangsu, China.
PeerJ. 2022 May 13;10:e13436. doi: 10.7717/peerj.13436. eCollection 2022.
Intimal hyperplasia is a common pathological process of restenosis following angioplasty, atherosclerosis, pulmonary hypertension, vein graft stenosis, and other proliferative diseases. This study aims to screen for potential novel gene targets and mechanisms related to vascular intimal hyperplasia through an integrated microarray analysis of the Gene Expression Omnibus Database (GEO) database.
The gene expression profile of the GSE56143 dataset was downloaded from the Gene Expression Omnibus database. Functional enrichment analysis, protein-protein interaction (PPI) network analysis, and the transcription factor (TF)-target gene regulatory network were used to reveal the biological functions of differential genes (DEGs). Furthermore, the expression levels of the top 10 key DEGs were verified at the mRNA and protein level in the carotid artery 7 days after ligation.
A total of 373 DEGs (199 upregulated DEGs and 174 downregulated DEGs) were screened. These DEGs were significantly enriched in biological processes, including immune system process, cell adhesion, and several pathways, which were mainly associated with cell adhesion molecules and the regulation of the actin cytoskeleton. The top 10 key DEGs (Ptprc, Fn1, Tyrobp, Emr1, Itgb2, Itgax, CD44, Ctss, Ly86, and Aif1) acted as key genes in the PPI network. The verification of these key DEGs at the mRNA and protein levels was consistent with the results of the above-mentioned bioinformatics analysis.
The present study identified key genes and pathways involved in intimal hyperplasia induced by carotid artery ligation. These results improved our understanding of the mechanisms underlying the development of intimal hyperplasia and provided candidate targets.
血管内膜增生是血管成形术后再狭窄、动脉粥样硬化、肺动脉高压、静脉移植物狭窄和其他增生性疾病的常见病理过程。本研究旨在通过整合基因表达综合数据库（GEO）数据库的基因芯片分析，筛选与血管内膜增生相关的潜在新基因靶点和机制。
从基因表达综合数据库中下载 GSE56143 数据集的基因表达谱。采用功能富集分析、蛋白质-蛋白质相互作用（PPI）网络分析和转录因子（TF）-靶基因调控网络，揭示差异基因（DEGs）的生物学功能。此外，在颈总动脉结扎后 7 天，在 mRNA 和蛋白质水平上验证了前 10 个关键 DEG 的表达水平。
筛选出 373 个 DEGs（199 个上调 DEGs 和 174 个下调 DEGs）。这些 DEGs 在生物学过程中显著富集，包括免疫系统过程、细胞黏附，以及几个途径，这些途径主要与细胞黏附分子和肌动蛋白细胞骨架的调节有关。前 10 个关键 DEGs（Ptprc、Fn1、Tyrobp、Emr1、Itgb2、Itgax、CD44、Ctss、Ly86 和 Aif1）作为 PPI 网络中的关键基因。这些关键 DEGs 在 mRNA 和蛋白质水平上的验证结果与上述生物信息学分析的结果一致。
本研究鉴定了颈动脉结扎诱导的内膜增生中涉及的关键基因和途径。这些结果提高了我们对内膜增生发展机制的理解，并为候选靶点提供了依据。
