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[1]贺王伟,张银芬,朱丽媛,等.小鼠巨噬细胞中microRNA-155促进急性心肌梗死后心室重构的作用机制[J].厦门大学学报(自然科学版),2018,57(05):650-657.[doi:10.6043/j.issn.0438-0479.201804028]
 HE Wangwei,ZHANG Yinfen,ZHU Liyuan,et al.Promoting Mechanism of MicroRNA-155 in Mouse Macrophages inVentricular Remodeling After Acute Myocardial Infarction[J].Journal of Xiamen University(Natural Science),2018,57(05):650-657.[doi:10.6043/j.issn.0438-0479.201804028]
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小鼠巨噬细胞中microRNA-155促进急性心肌梗死后心室重构的作用机制(PDF/HTML)
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《厦门大学学报(自然科学版)》[ISSN:0438-0479/CN:35-1070/N]

卷:
57卷
期数:
2018年05期
页码:
650-657
栏目:
研究论文
出版日期:
2018-09-27

文章信息/Info

Title:
Promoting Mechanism of MicroRNA-155 in Mouse Macrophages inVentricular Remodeling After Acute Myocardial Infarction
文章编号:
0438-0479(2018)05-0650-08
作者:
贺王伟张银芬朱丽媛黄 宇谢 强*
厦门大学附属第一医院心血管内科,福建 厦门 361003
Author(s):
HE WangweiZHANG YinfenZHU LiyuanHUANG YuXIE Qiang*
Department of Cardiology,the First Affiliated Hospital of Xiamen University,Xiamen 361003,China
关键词:
巨噬细胞 急性心肌梗死 microRNA-155 炎症因子 心室重构
Keywords:
macrophage acute myocardial infarction microRNA-155 inflammatory factor ventricular remodeling
分类号:
R 541
DOI:
10.6043/j.issn.0438-0479.201804028
文献标志码:
A
摘要:
为探究巨噬细胞中microRNA-155(miR-155)表达水平对急性心肌梗死(AMI)后心室重构的影响及其机制,将miR-155基因过表达(miR-155+/+)和基因敲除(miR-155-/-)小鼠的骨髓细胞分别移植给野生型(WT)小鼠进行血液重建,并建立AMI模型,检测血浆及心肌组织中炎症因子TNF-α和IL-10的表达水平,评价小鼠心脏功能并观察巨噬细胞浸润、心室重构的情况,进而利用病毒包装技术敲降细胞因子信号传导抑制蛋白1(SOCS1)基因后验证其作为miR-155靶基因的影响.结果显示:miR-155+/+组较miR-155-/-组小鼠的心脏收缩功能显著受限(p<0.01); 巨噬细胞中miR-155表达水平显著影响血浆中炎症因子的释放(p<0.01),并促进心室重构的发生(p<0.01); miR-155表达水平与SOCS1的mRNA及蛋白质表达水平呈显著负相关(p<0.01).综上可知,抑制AMI后巨噬细胞中miR-155的表达可以促进靶基因SOCS1的表达,从而减轻AMI后的炎症反应,有利于减轻心室重构.
Abstract:
To investigate the effect of microRNA-155(miR-155)expression in macrophages on ventricular remodeling after acute myocardial infarction(AMI)and its mechanism,miR-155+/+ and miR-155-/- mouse bone marrow cells were transplanted to the wild type mice for blood reconstruction and the AMI model was established.In this study,the levels of inflammatory factors TNF-α and IL-10 in plasma were detected,and the cardiac function of mice,macrophage infiltration and ventricular remodeling were observed.In addition,the SOCS1 gene was knocked down with virus packagingtechnology to verify the function of SOCS1 as the target regulatorygene of miR-155.Theresults showed as following:the systolic function of miR-155+/+ group was significantly lower than that of miR-155-/- group(p<0.01).MiR-155 significantly affected the release of inflammatory factors in plasma(p<0.01),and promoted the occurrence of ventricular remodeling(p<0.01).Moreover,the expression level of miR-155 was negatively correlated with SOCS1 mRNA and protein expression(p<0.01).In conclusion,inhibition of the expression of miR-155 in macro-phages after AMI can promote the expression of target gene SOCS1 and reduce the inflammatory reaction after AMI,which will be beneficial to reduce ventricular remodeling.

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备注/Memo

备注/Memo:
收稿日期:2018-04-30 录用日期:2018-07-02
基金项目:福建省科技计划项目(2014D023)
*通信作者:arthur2014@sina.com
引文格式:贺王伟,张银芬,朱丽媛,等.小鼠巨噬细胞中microRNA-155促进急性心肌梗死后心室重构的作用机制[J].厦门大学学报(自然科学版),2018,57(5):650-657.
Citation:HE W W,ZHANG Y F,ZHU L Y,et al. Promoting mechanism of microRNA-155 in mouse macrophages in ventricular remodeling after acute myocardial infarction[J].J Xiamen Univ Nat Sci,2018,57(5):650-657.(in Chinese)
更新日期/Last Update: 1900-01-01