Department of Vascular Surgery, Jining Medical University Affiliated Jining No. 1 People's Hospital.
Department of Cardiovascular Medicine, Affiliated Hospital of Jining Medical University.
Int Heart J. 2024 Sep 30;65(5):945-955. doi: 10.1536/ihj.24-062. Epub 2024 Sep 12.
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.
血管内过度的新生内膜增生（NIH）是经皮冠状动脉介入治疗（PCI）后再狭窄（RS）的主要原因。本研究旨在建立大鼠颈动脉球囊损伤模型，鉴定与 NIH 相关的调控基因。
我们建立了大鼠模型并进行了 RNA 测序，以鉴定差异表达的长链非编码 RNA（DElncRNA）和差异表达的信使 RNA（DEmRNA）。使用小鼠微环境细胞计数器分析免疫细胞。分析了 DEmRNA、DElncRNA 和免疫细胞之间的 Pearson 相关性，然后进行功能富集分析。使用 Cytoscape 识别核心 DEmRNA。接下来，构建了核心 lncRNA-mRNA-免疫细胞调控网络。从基因表达综合数据库和基因卡片数据库中获取 NIH 相关基因集进行验证。
在大鼠颈动脉组织中鉴定出 2165 个 DEmRNA 和 705 个 DElncRNA。筛选出 4 种关键免疫细胞，包括肥大细胞、血管、内皮细胞和成纤维细胞。基于 DEmRNA、DElncRNA 和 4 种关键免疫细胞之间的 Pearson 相关性，获得了 246 个 DEmRNA 和 93 个 DElncRNA。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 lncRNA-mRNA-免疫细胞调控网络，包括 9 个 mRNAs、4 个 lncRNAs 和成纤维细胞。外部数据集验证证实了这些 mRNAs 和 lncRNAs 与 NIH 的显著相关性。
在这项研究中，构建了一个与 NIH 相关的 lncRNA-mRNA-免疫细胞调控网络，为探索心血管疾病中 RS 的潜在机制提供了线索。
