Recent studies have shed light on the involvement of long non-coding RNAs (lncRNAs) in the initiation and development of stroke. However, the regulatory function of many lncRNAs in large artery atherosclerosis (LAA) has not been fully elucidated. Based on the competing endogenous RNA (ceRNA) hypothesis recently proposed by Pandolfi, the present study was conducted using experimental techniques and bioinformatics to investigate the expression and regulatory function of a lncRNA involved in the development of LAA. The lncRNAs differentially expressed in stroke were obtained using meta-analysis, and one lncRNA was selected for experimental studies on patients with LAA (n = 100) and healthy controls (n = 100) using quantitative real-time polymerase chain reaction (qRT-PCR). The patients were also evaluated through meta-analysis to identify the function of the selected lncRNA, miRNAs, and mRNAs with altered expression in stroke. Finally, the experimental results and meta-analysis findings were integrated, and different functional groups were assigned. The results indicated that the level of lncRNA-RUNX1-IT1 was significantly lower in the patients with LAA compared to the healthy control subjects (p > 0.05). Logistic regression analyses revealed that the expression of lncRNA-RUNX1-IT1 was inversely correlated with LAA (P = 009, OR = 0.871, 95% CI: 0.786–0.965). In addition, a network of differentially expressed genes (DE genes) was created for miRNAs and mRNAs based on their association with lncRNA-RUNX1-IT1. Functional analysis showed that the DE genes in the network are involved in the apoptosis and alternative splicing of RNAs. The findings of the present study suggest that the downregulation of lncRNA-RUNX1-IT1 is associated with LAA development by interrupting the regulatory network of cells. The results of network analysis demonstrated that the lncRNA-RUNX1-IT1 could influence the expression of mRNAs and miRNAs involved in the apoptosis and alternative splicing of RNAs.

最近的研究阐明了长链非编码 RNA (lncRNA) 参与中风的发生和发展。然而，许多lncRNA在大动脉粥样硬化（LAA）中的调节功能尚未完全阐明。基于 Pandolfi 最近提出的竞争性内源 RNA (ceRNA) 假说，本研究使用实验技术和生物信息学来研究参与 LAA 发展的 lncRNA 的表达和调节功能。使用meta分析获得卒中中差异表达的lncRNA，并选择1个lncRNA用于LAA患者（n  = 100）和健康对照（n = 100) 使用定量实时聚合酶链反应 (qRT-PCR)。还通过荟萃分析对患者进行了评估，以确定所选 lncRNA、miRNA 和 mRNA 在中风中表达改变的功能。最后，整合实验结果和荟萃分析结果，分配不同的功能组。结果表明，与健康对照组相比，LAA 患者的 lncRNA-RUNX1-IT1 水平显着降低（p  > 0.05）。Logistic回归分析显示lncRNA-RUNX1-IT1的表达与LAA呈负相关（P = 009，OR = 0.871，95% CI：0.786–0.965）。此外，基于它们与 lncRNA-RUNX1-IT1 的关联，为 miRNA 和 mRNA 创建了一个差异表达基因（DE 基因）网络。功能分析表明，网络中的DE基因参与了RNA的凋亡和选择性剪接。本研究的结果表明，lncRNA-RUNX1-IT1 的下调通过中断细胞的调节网络与 LAA 的发展有关。网络分析结果表明，lncRNA-RUNX1-IT1可以影响参与RNA凋亡和选择性剪接的mRNA和miRNA的表达。