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首页> 外文期刊>Thrombosis Research: An International Journal on Vascular Obstruction, Hemorrhage and Hemostasis >Downregulation of let-7e-5p contributes to endothelial progenitor cell dysfunction in deep vein thrombosis via targeting FASLG
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Downregulation of let-7e-5p contributes to endothelial progenitor cell dysfunction in deep vein thrombosis via targeting FASLG

机译:let-7e-5p的下调通过靶向FASLG促进深静脉血栓形成中的内皮祖细胞功能障碍

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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 over-expressing 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. (C) 2015 Elsevier Ltd. All rights reserved.
机译:这项研究旨在评估let-7e-5p在内皮祖细胞(EPC)功能中的作用,并探讨其对深静脉血栓形成(DVT)的治疗潜力。我们进行了miRNA筛选,发现与对照组相比,DVT患者的let-7e-5p被下调。通过使用let-7e-5p agomir和antagomir,我们证明了let-7e-5p增加了人和大鼠EPC的迁移和管形成。基于生物信息学,荧光素酶报告基因测定和基因表达分析,我们确定了Fas配体(FASLG)作为let-7e-5p的目标,而FASLG敲低增加了EPC的迁移和管形成。此外,在大鼠静脉血栓形成模型中,过表达let-7e-5p的EPC表现出增强的归巢和血栓血运重建能力。总之,let-7e-5p调节EPC的功能,并且是DVT治疗中的潜在治疗靶标。 (C)2015 Elsevier Ltd.保留所有权利。

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