LncRNA DLEU1 promotes angiogenesis in diabetic foot ulcer wound healing by regulating miR-96-5p

被引:3
作者
Yang, Meiying [1 ]
Gu, Yufang [2 ]
机构
[1] Zibo Cent Hosp, Dept Trauma Orthoped, 10 Shanghai Rd, Zibo 255000, Peoples R China
[2] Zibo Cent Hosp, Dept Gastrointestinal Surg, Zibo 255000, Peoples R China
关键词
Diabetic foot ulcer; Human umbilical vein endothelial cells; miR-96-5p; ncRNA DLEU1; Serum biomarkers; EPIDEMIOLOGY;
D O I
10.1007/s11845-023-03471-x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BackgroundDiabetic foot ulcer (DFU) carries high rates of major amputation and mortality.AimsThe goals of this study were to identify expression of circulating lncRNA DLEU1 and miR-96-5p in patients with diabetic foot ulcer (DFU) and to explore the function of lncRNA DLEU1/miR-96-5p axis in DFU.MethodsMatched patients with DFU and healthy individuals were randomly selected. Serum samples from all subjects were used for circulating lncRNA DLEU1 and miR-96-5p assessment by RT-qPCR. Receiver operating characteristic (ROC) curve was plotted to assess the discriminative capacity of lncRNA DLEU1 and miR-96-5p in identifying DFU. Cell proliferation was detected by CCK-8 assay. Cell apoptosis was assayed by Annexin V-FITC/PI staining method. Bioinformatics, luciferase reporter activity assay, and in vitro cell experiments were used to explore the relationship between lncRNA DLEU1 and miR-96-5p.ResultsLncRNA DLEU1 and miR-96-5p were significantly up- and downregulated in patients with DFU, respectively, compared with controls. After ROC assessment, lncRNA DLEU1 and miR-96-5p were found to discriminate DFU from miR-96-5p. Furthermore, lncRNA DLEU1 inhibited human umbilical vein endothelial cells (HUVECs) cell proliferation and increased HUVECs apoptosis and oxidative stress through sponging miR-96-5p.ConclusionOur findings suggest lncRNA DLEU1 and miR-96-5p as circulating biomarkers for DFU. Also, we provide the clue for the pathogenic significance of lncRNA DLEU1/miR-96-5p in DFU, as well as insights for new potential targets.
引用
收藏
页码:241 / 247
页数:7
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