Endothelial progenitor cell (EPC) recruitment and angiogenesis play crucial roles in aneurysm neck endothelialization, but the mechanisms of EPC recruitment and angiogenesis are still unclear. Recent studies have shown that long noncoding RNAs (lncRNAs) can regulate the function and differentiation of cells in various ways. LncRNA TUG1 is involved in liver cancer and glioma-mediated angiogenesis. The aim of this study was to investigate the role of lncRNA TUG1 in regulating EPC migration and differentiation. Overexpression and knockdown of lncRNA TUG1 with lentivirus, scratch assays, Transwell assays and tube formation assays using EPCs isolated from rat bone marrow showed that lncRNA TUG1 overexpression promoted EPC migration, invasion and differentiation. Moreover, ELISAs showed that lncRNA TUG1 overexpression increased VEGF expression. Bioinformatics prediction, luciferase assays, Western blots and RIP assays indicated that lncRNA TUG1 functions as a ceRNA (competing endogenous RNA) for miR-6321 and that miR-6321 inhibits EPC migration and differentiation through its target, ATF2. As a potential therapeutic target, lncRNA TUG1 may play a vital role in the pathogenesis of aneurysms.

中文翻译：

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LncRNA TUG1充当miR-6321的ceRNA，以促进内皮祖细胞的迁移和分化。

内皮祖细胞（EPC）募集和血管生成在动脉瘤颈内皮化中起着关键作用，但EPC募集和血管生成的机制仍不清楚。最近的研究表明，长的非编码RNA（lncRNA）可以通过多种方式调节细胞的功能和分化。LncRNA TUG1参与肝癌和神经胶质瘤介导的血管生成。这项研究的目的是调查lncRNA TUG1在调节EPC迁移和分化中的作用。lncRNA TUG1在慢病毒中的过表达和敲除，划痕分析，Transwell分析和使用从大鼠骨髓中分离得到的EPC进行的管形成分析表明，lncRNA TUG1过表达促进了EPC的迁移，侵袭和分化。而且，ELISA显示lncRNA TUG1过表达增加了VEGF的表达。生物信息学预测，荧光素酶测定，Western印迹和RIP测定表明，lncRNA TUG1充当miR-6321的ceRNA（竞争内源性RNA），miR-6321抑制EPC通过其靶标ATF2迁移和分化。作为潜在的治疗靶标，lncRNA TUG1可能在动脉瘤的发病机理中起着至关重要的作用。