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microRNA let-7e-5p通过靶向Fas 配体(FASLG)调控内皮祖细胞功能
发布日期:2017-08-15 11:13:12

Thromb Res. 2016 Feb;138:30-6. doi: 10.1016/j.thromres.2015.12.020. Epub 2015 Dec 24.
Downregulation of let-7e-5p contributes to endothelial progenitor cell dysfunction in deep vein thrombosis via targeting FASLG.
Kong L, Du X, Hu N, Li W, Wang W, Wei S, Zhuang H, Li X, Li C.

Abstract
      This study aimed to evaluate the role  of let-7e-5p in endothelial progenitor cells (EPCs) function and explore its therapeutic potential for deep vein thrombosis (DVT). We performed miRNAs screening and found that let-7e-5p was downregulated in DVT patients compared to control subjects. By using let-7e-5p agomir and antagomir, we demonstrated that let-7e-5p increased the migration and tube formation of human and rat EPCs. Based on bioinformatics, luciferase reporter assay and gene expression analysis, we identified Fas ligand (FASLG) as the target of let-7e-5p, and FASLG knockdown increased the migration and tube formation of EPCs. Furthermore, EPCs overexpressing let-7e-5p exhibited enhanced ability of homing and thrombus revascularization in rat model of venous thrombosis. In conclusion, let-7e-5p regulates the function of EPCs and is a potential therapeutic target in DVT treatment.
      内皮祖细胞在深静脉血栓的再通过程中起重要作用,为了研究microRNA let-7e-5p 在内皮祖细胞中的功能和作为DVT治疗作用靶标的潜能,我们通过高通量筛选鉴定,let-7e-5p 在DVT病人中表达下调;通过递送microRNA let-7e-5p 激动剂和拮抗剂增加或敲低其表达,探讨其生物学功能。研究结果表明let-7e-5p 通过调控其靶基因Fas ligand (FASLG)来调控内皮祖细胞的细胞迁移能力、血管形成能力以及凋亡增加。构建大鼠血栓模型,体内实验结果表明let-7e-5p能促进EPC细胞归巢和血栓血管重塑 。let-7e-5p调控内皮祖细胞的功能,可能作为新的深静脉血栓形成治疗靶标。

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