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小分子非编码RNA miR-483-3p通过作用血清应答因子调控内皮祖细胞的功能
发布日期:2017-08-15 11:25:24

J Transl Med. 2016 Jan 22;14:23.
Upregulation of miR-483-3p contributes to endothelial progenitor cells dysfunction in deep veinthrombosis patients via SRF.
Kong L, Hu N, Du X, Wang W, Chen H, Li W, Wei S, Zhuang H, Li X, Li C.

Abstract
      Endothelial progenitor cells (EPCs) contribute to recanalization of deep vein thrombosis (DVT). This study aimed to detect miRNA expression profiles in EPCs from patients with DVT and characterize the role of miRNA in EPCs dysfunction. We identified miR-483-3p as a candidate miRNA upregulated in EPCs from DVT patients. By using miR-483-3p agomir and antagomir, we demonstrated that miR-483-3p decreased the migration and tube formation while increased the apoptosis of EPCs. Moreover, we identified serum response factor (SRF) as the target of miR-483-3p, and showed that SRF knockdown decreased the migration and tube formation while increased the apoptosis of EPCs. In addition, miR-483-3p inhibition led to enhanced ability of homing and thrombus resolution of EPCs in rat model of venous thrombosis. Our results demonstrated that miR-483-3p is upregulated in EPCs from DVT patients, and it targets SRF to decrease EPCs migration and tube formation and increase apoptosis in vitro, while decrease EPCs homing and thrombus resolution in vivo. MiR-483-3p 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,我们发现小分子非编码RNA mir-483-3p在DVT病人来源的内皮祖细胞中高表达,通过递送mir-483-3p激动剂和拮抗剂增加或敲低其表达,探讨mir-483-3p的生物学功能。研究结果表明mir-483-3p通过调控其靶基因血清应答因子(serum response factor ,SRF)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。通过构建大鼠血栓模型,证实mir-483-3p参与了血栓机化再通过程。mir-483-3p可能作为新的深静脉血栓形成治疗靶标。

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