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首页> 外文期刊>Kaohsiung Journal of Medical Sciences >Regulatory effects of miR-146a/b on the function of endothelial progenitor cells in acute ischemic stroke in mice
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Regulatory effects of miR-146a/b on the function of endothelial progenitor cells in acute ischemic stroke in mice

机译：miR-146a / b对小鼠急性缺血性卒中内皮祖细胞功能的调节作用

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The study aims to explore how microRNA-146a/b (miR-146a/b) regulates the function of endothelial progenitor cells (EPCs) in acute ischemic stroke in mice. Eighty male SPF C57BL/6J mice were evenly divided into the model-6?h, model-12?h, model-24?h (mice suffered from middle cerebral artery occlusion [MCAO] for 6?h, 12?h and model-24?h) and normal groups. EPCs were transfected and assigned into the control, MCAO, MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups. The qRT-PCR was used to detect miR-146a/b expression in EPCs. Expressions of tumor necrosis factor receptor-associated factor 6 (TRAF6) and interleukin-1 receptor-associated kinase 1 (IRAK1) were detected using western blotting. Cell proliferation and migration of EPCs were testified using CCK-8 assay and scratch test, respectively. Angiogenesis ability of EPCs was observed under microscope. MiR-146a and miR-146b expressions were lower in the model groups than the normal group. There were up-regulated TRAF6 and IRAK1 expressions in the model-6?h, model-12?h and model-24?h groups compared with the normal group. And there were down-regulated TRAF6 and IRAK1 expressions in the MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups than in the MCAO group. Compared with the control group, the proliferation, migration and angiogenesis ability of EPCs were significantly lower in the MCAO group, but higher in the MCAO-miR-146a, MCAO-miR-146b and MCAO-miR-146a/b groups. Besides, the miR-146a/b group showed more enhancement than the MCAO-miR-146a and MCAO-miR-146b groups. MiR-146a/b could down-regulate the TRAF6 and IRAK1 expressions and promote proliferation, migration and angiogenesis ability of EPCs, which was important for recovery of patients with hyperacute ischemic stroke.
机译：这项研究旨在探讨microRNA-146a / b（miR-146a / b）在小鼠急性缺血性中风中如何调节内皮祖细胞（EPC）的功能。将80只SPF C57BL / 6J雄性小鼠平均分为模型6？h，模型12？h，模型24？h（患有大脑中动脉闭塞[MCAO]的小鼠6？h，12？h和模型）。 -24？h）和正常人群。将EPC转染并分为对照组MCAO，MCAO-miR-146a，MCAO-miR-146b和MCAO-miR-146a / b组。使用qRT-PCR检测EPC中的miR-146a / b表达。使用western blotting检测肿瘤坏死因子受体相关因子6（TRAF6）和白介素1受体相关激酶1（IRAK1）的表达。 EPC的细胞增殖和迁移分别使用CCK-8分析和刮擦测试进行了验证。在显微镜下观察了EPC的血管生成能力。模型组中的MiR-146a和miR-146b表达低于正常组。与正常组相比，模型6？h，模型12？h和模型24？h组的TRAF6和IRAK1表达上调。与MCAO组相比，MCAO-miR-146a，MCAO-miR-146b和MCAO-miR-146a / b组的TRAF6和IRAK1表达下调。与对照组相比，MCAO组中EPCs的增殖，迁移和血管生成能力明显降低，而MCAO-miR-146a，MCAO-miR-146b和MCAO-miR-146a / b组则较高。此外，miR-146a / b组比MCAO-miR-146a和MCAO-miR-146b组表现出更多的增强作用。 MiR-146a / b可以下调TRAF6和IRAK1的表达，并促进EPC的增殖，迁移和血管生成能力，这对于恢复急性缺血性卒中的患者非常重要。

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