Identification of the Neointimal Hyperplasia-Related LncRNA-mRNA-Immune Cell Regulatory Network in a Rat Carotid Artery Balloon Injury Model

IF 1.2 4区医学 Q3 CARDIAC & CARDIOVASCULAR SYSTEMS International heart journal Pub Date : 2024-09-12 DOI:10.1536/ihj.24-062

Yuan Gou, Anli Zhao, Tao Qin, Bin Yang

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Abstract

Excessive neointimal hyperplasia (NIH) of coronary vessels in patients is the main cause of restenosis (RS) after percutaneous coronary intervention (PCI). This study aimed to identify the regulatory genes related to NIH in a rat carotid artery balloon injury model.

We established a rat model and performed RNA sequencing to identify differentially expressed long non-coding RNAs (DElncRNAs) and differentially expressed message RNAs (DEmRNAs). Immune cells were analyzed using a murine Microenvironment Cell Population counter. The Pearson correlation between DEmRNAs, DElncRNAs, and immune cells was analyzed, followed by function enrichment analysis. Core DEmRNA was identified using Cytoscape. Next, a core lncRNAs-mRNAs-immune cell regulatory network was constructed. NIH-related gene sets from the Gene Expression Omnibus and GeneCards databases were used for validation.

A total of 2,165 DEmRNAs and 705 DElncRNAs were identified in rat carotid artery tissue. Four key immune cells were screened out, including mast cells, vessels, endothelial cells, and fibroblasts. Based on the Pearson correlation between DEmRNAs, DElncRNAs and 4 key immune cells, 246 DEmRNAs and 93 DElncRNAs were obtained. DEmRNAs that interact with lncRNAs were mainly involved in the cell cycle, MAPK signaling pathway, and PI3K-Akt signaling pathway. A core lncRNA-mRNA-immune cell regulatory network was constructed, including 9 mRNAs, 4 lncRNAs, and fibroblasts. External datasets validation confirmed the significant correlation of both these mRNAs and lncRNAs with NIH.

In this study, an lncRNA-mRNA-immune cell regulatory network related to NIH was constructed, which provided clues for exploring the potential mechanism of RS in cardiovascular diseases.

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在大鼠颈动脉球囊损伤模型中鉴定与新内膜增生相关的 LncRNA-mRNA 免疫细胞调控网络

患者冠状动脉血管的过度新内膜增生（NIH）是经皮冠状动脉介入治疗（PCI）后再狭窄（RS）的主要原因。本研究旨在鉴定大鼠颈动脉球囊损伤模型中与 NIH 相关的调控基因。我们建立了一个大鼠模型并进行了 RNA 测序，以鉴定差异表达的长非编码 RNA（DElncRNA）和差异表达的信息 RNA（DEmRNA）。使用小鼠微环境细胞群计数器对免疫细胞进行了分析。分析了 DEmRNA、DElncRNA 和免疫细胞之间的皮尔逊相关性，然后进行了功能富集分析。使用 Cytoscape 对核心 DEmRNA 进行了鉴定。接着，构建了核心lncRNAs-mRNAs-免疫细胞调控网络。大鼠颈动脉组织中共鉴定出 2,165 个 DEmRNA 和 705 个 DElncRNA。筛选出了肥大细胞、血管、内皮细胞和成纤维细胞等四种关键免疫细胞。根据 DEmRNAs、DElncRNAs 和 4 个关键免疫细胞之间的皮尔逊相关性，得到了 246 个 DEmRNAs 和 93 个 DElncRNAs。与lncRNA相互作用的DEmRNA主要参与细胞周期、MAPK信号通路和PI3K-Akt信号通路。构建了一个核心的lncRNA-mRNA-免疫细胞调控网络，包括9个mRNA、4个lncRNA和成纤维细胞。这项研究构建了一个与NIH相关的lncRNA-mRNA-免疫细胞调控网络，为探索RS在心血管疾病中的潜在机制提供了线索。

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来源期刊

International heart journal 医学-心血管系统

CiteScore

2.50

自引率

6.70%

发文量

148

审稿时长

6-12 weeks

期刊介绍： Authors of research articles should disclose at the time of submission any financial arrangement they may have with a company whose product figures prominently in the submitted manuscript or with a company making a competing product. Such information will be held in confidence while the paper is under review and will not influence the editorial decision, but if the article is accepted for publication, the editors will usually discuss with the authors the manner in which such information is to be communicated to the reader.