Studies have shown that miR-217 can induce cell senescence, but its mechanism of action in vascular endothelial cell senescence is less reported. Therefore, this study aimed to investigate how miR-217 plays a role in endothelial cell senescence. Human umbilical vein endothelial cells (HUVECs) were used to replicate the aging model, and the population doubling levels (PDLs) during cell passage were counted. Senescence-associated β-galactosidase (SA-β-gal) staining, Real-time quantitative PCR (RT-qPCR), MTT assay, Transwell, and tube formation were used to detect the effects of miR-217 on young and senescent HUVECs. Targetscan7.2 and luciferase assay predicted and verified the relationship between miR-217 and the target gene, and the expression of silent information regulator 1 (SIRT1) and p53 was detected by RT-qPCR and western blot. In addition, SA-β-gal staining detected the effects of miR-217 inhibitor and SIRT1 on senescent HUVECs. MiR-217 was upregulated in senescent endothelial cells. Overexpression of miR-217 promoted the increase of SA-β-gal positive cells, and inhibited proliferation, migration and angiogenesis during endothelial cell growth. Furthermore, SIRT1 was a target gene of miR-217. Simultaneous silencing of SIRT1 reversed the effect of miR-217 inhibitor on the reduction of SA-β-gal positive-staining cells. Our data suggest that overexpression of miR-217 promoted vascular endothelial cell senescence by targeting the SIRT1/p53 signaling pathway, which may provide a new basis for studying the mechanism of action in vascular endothelial cell senescence.

研究表明miR-217可以诱导细胞衰老，但其在血管内皮细胞衰老中的作用机制报道较少。因此，本研究旨在探讨miR-217如何在内皮细胞衰老中发挥作用。使用人脐静脉内皮细胞（HUVEC）复制衰老模型，并对细胞传代过程中的群体倍增水平（PDL）进行计数。采用衰老相关β-半乳糖苷酶（SA-β-gal）染色、实时定量PCR（RT-qPCR）、MTT测定、Transwell和成管法检测miR-217对年轻和衰老HUVEC的影响。Targetscan7.2和荧光素酶检测预测并验证miR-217与靶基因的关系，并通过RT-qPCR和western blot检测沉默信息调节因子1（SIRT1）和p53的表达。此外，SA-β-gal染色检测miR-217抑制剂和SIRT1对衰老HUVEC的影响。MiR-217 在衰老内皮细胞中上调。miR-217的过表达促进SA-β-gal阳性细胞的增加，并抑制内皮细胞生长过程中的增殖、迁移和血管生成。此外，SIRT1是miR-217的靶基因。同时沉默 SIRT1 可逆转 miR-217 抑制剂对 SA-β-gal 阳性染色细胞减少的影响。我们的数据表明，miR-217的过表达通过靶向SIRT1/p53信号通路促进血管内皮细胞衰老，这可能为研究血管内皮细胞衰老的作用机制提供新的基础。MiR-217 在衰老内皮细胞中上调。miR-217的过表达促进SA-β-gal阳性细胞的增加，并抑制内皮细胞生长过程中的增殖、迁移和血管生成。此外，SIRT1是miR-217的靶基因。同时沉默 SIRT1 可逆转 miR-217 抑制剂对 SA-β-gal 阳性染色细胞减少的影响。我们的数据表明，miR-217的过表达通过靶向SIRT1/p53信号通路促进血管内皮细胞衰老，这可能为研究血管内皮细胞衰老的作用机制提供新的基础。MiR-217 在衰老内皮细胞中上调。miR-217的过表达促进SA-β-gal阳性细胞的增加，并抑制内皮细胞生长过程中的增殖、迁移和血管生成。此外，SIRT1是miR-217的靶基因。同时沉默 SIRT1 可逆转 miR-217 抑制剂对 SA-β-gal 阳性染色细胞减少的影响。我们的数据表明，miR-217的过表达通过靶向SIRT1/p53信号通路促进血管内皮细胞衰老，这可能为研究血管内皮细胞衰老的作用机制提供新的基础。SIRT1 是 miR-217 的靶基因。同时沉默 SIRT1 可逆转 miR-217 抑制剂对 SA-β-gal 阳性染色细胞减少的影响。我们的数据表明，miR-217的过表达通过靶向SIRT1/p53信号通路促进血管内皮细胞衰老，这可能为研究血管内皮细胞衰老的作用机制提供新的基础。SIRT1 是 miR-217 的靶基因。同时沉默 SIRT1 可逆转 miR-217 抑制剂对 SA-β-gal 阳性染色细胞减少的影响。我们的数据表明，miR-217的过表达通过靶向SIRT1/p53信号通路促进血管内皮细胞衰老，这可能为研究血管内皮细胞衰老的作用机制提供新的基础。