Atherosclerosis (AS) is the main pathological basis of coronary heart disease, cerebral infarction and peripheral vascular disease, which seriously endanger people’s life and health. In recent years, long non-coding RNA (lncRNA) has been found to be involved in gene expression regulation, but the research on AS is still in the initial stage. In this study, we mainly studied the role of HCG11 in patients with AS. Quantitative Real-time Polymerase Chain Reaction (QRT-PCR) was used to detect the expression of HCG11 and miR-144 in the serum of AS patients and healthy volunteers. Oxidation Low Lipoprotein (Ox-LDL), interleukin-6 (IL-6) and tumor necrosis factor α (TNF α) radiation were used to establish human vascular smooth muscle cells (VSMCs) in vitro model. Cell proliferation was determined by Cell Counting Kit-8 (CCK-8) assay. The apoptosis rate was determined by flow cytometry (FACS) and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL) staining. The expression levels of Forkhead box protein F1 (FOXF1), B cell lymphoma-2 (Bcl-2) and BCL2-Associated X (Bax) were detected by qRT-PCR. Luciferase gene reporter and RNA pull down experiments confirmed the relationship between HCG11 and miR-144, miR-144 and FOXF1. This study showed that HCG11 was significantly upregulated in patients with AS, while miR-144 was down-regulated in patients with AS. Ox-LDL and IL-6 in VSMCs induced up-regulation of HCG11 and down-regulation of miR-144. Overexpression of HCG11 promoted the proliferation and inhibited apoptosis of VSMCs. Luciferase gene reporter gene assay showed that HCG11 could bind to miR-144, and miR-144 could bind to FOXF1. Overexpression of miR-144 reversed the effect of HCG11 on VSMCs. LncRNA HCG11 regulates proliferation and apoptosis of vascular smooth muscle cell through targeting miR-144-3p/FOXF1 axis.

中文翻译：

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LncRNA HCG11通过靶向miR-144-3p/FOXF1轴调节动脉粥样硬化血管平滑肌细胞的增殖和凋亡


动脉粥样硬化（AS）是冠心病、脑梗塞及周围血管疾病的主要病理基础，严重危害人们的生命健康。近年来，人们发现长链非编码RNA（lncRNA）参与基因表达调控，但对AS的研究仍处于起步阶段。本研究主要研究HCG11在AS患者中的作用。采用实时定量聚合酶链反应（QRT-PCR）检测AS患者和健康志愿者血清中HCG11和miR-144的表达。采用氧化低脂蛋白（Ox-LDL）、白细胞介素6（IL-6）和肿瘤坏死因子α（TNFα）辐射建立人血管平滑肌细胞（VSMC）体外模型。通过细胞计数试剂盒-8 (CCK-8) 测定法测定细胞增殖。通过流式细胞术（FACS）和末端脱氧核苷酸转移酶介导的dUTP-生物素缺口末端标记测定（TUNEL）染色测定细胞凋亡率。采用qRT-PCR检测Forkhead box蛋白F1（FOXF1）、B细胞淋巴瘤-2（Bcl-2）和BCL2相关X（Bax）的表达水平。荧光素酶基因报告基因和RNA pull down实验证实了HCG11与miR-144、miR-144与FOXF1之间的关系。这项研究表明，AS 患者中 HCG11 显着上调，而 miR-144 在 AS 患者中下调。 VSMC 中的 Ox-LDL 和 IL-6 诱导 HCG11 上调和 miR-144 下调。 HCG11的过表达促进VSMCs的增殖并抑制其凋亡。荧光素酶基因报告基因检测显示HCG11可以与miR-144结合，miR-144可以与FOXF1结合。 miR-144 的过度表达逆转了 HCG11 对 VSMC 的影响。 LncRNA HCG11通过靶向miR-144-3p/FOXF1轴调节血管平滑肌细胞的增殖和凋亡。