>
网站首页期刊介绍通知公告编 委 会投稿须知电子期刊广告合作联系我们
最新消息:
microRNA-150在心房颤动患者心房组织中的表达及其对大鼠H9c2心肌细胞的影响
作者:李小兵  王军  吕瑛  张会军  黄建成  李红英  苏振宇 
单位:河北医科大学第一医院 心脏外科, 河北 石家庄 050031
关键词:microRNA-150 心房颤动 心肌细胞 胶原Ⅰ 基质金属蛋白酶-9 转化生长因子-β1 大鼠 
分类号:R-33;R541.75
出版年·卷·期(页码):2018·37·第四期(612-616)
摘要:

目的:探讨microRNA-150在心房颤动患者心房组织中的表达及其对大鼠H9c2心肌细胞的影响。方法:选择行风湿性心脏病瓣膜置换术心房颤动患者的心房组织(30例)作为心房颤动组,行风湿性心脏病瓣膜置换术窦性心律患者的心房组织(30例)作为对照组。将H9c2心肌细胞分为microRNA-150组(转染pGIPZ-miR-150慢病毒)、阴性对照组(转染pGIPZ慢病毒)和空白对照组(未转染病毒)。采用RT-PCR测定组织和细胞中microRNA-150表达和cMyb mRNA水平;采用Western blotting测定细胞中cMyb蛋白、基质金属蛋白酶-9(MMP-9)和转化生长因子-β1(TGF-β1)水平;采用ELISA法测定细胞中胶原Ⅰ水平。结果:心房颤动组心房组织中microRNA-150的相对表达量低于对照组(P<0.05)。microRNA-150组H9c2心肌细胞中microRNA-150表达量明显高于阴性对照组和空白对照组(P<0.05),cMyb mRNA和蛋白水平明显低于阴性对照组和空白对照组(P<0.05),胶原Ⅰ水平明显低于阴性对照组和空白对照组(P<0.05),MMP-9和TGF-β1水平明显低于阴性对照组和空白对照组(P<0.05);阴性对照组和空白对照组H9c2心肌细胞中各指标差异无统计学意义(P>0.05)。结论:心房颤动患者心房组织中microRNA-150表达量下降,上调心肌细胞中microRNA-150表达量可通过靶基因cMyb降低心肌细胞纤维化。

Objective:To investigate the expression of microRNA-150 in atrial fibrillation and its effect on rat H9c2 cardiomyocytes.Methods:30 cases of atrial tissue of patients with atrial fibrillation who underwent valve replacement were treated as atrial fibrillation group, and 30 cases of atrial tissue of patients with sinus thythun receiving valve replacement were selected as control group.H9c2 cardiomyocytes were divided into microRNA-150 group (transfected with pGIPZ-miR-150 lentivirus), negative control group (transfected with pGIPZ lentivirus) and blank control group (untransfected virus).The expression of microRNA-150 and cMyb mRNA in tissues and cells were determined by RT-PCR. The levels of cMyb protein, matrix metalloproteinase-9 (MMP-9) and transforming growth factor-β1 (TGF-β1) were measured by Western blotting. The level of collagen Ⅰ in cells was determined by ELISA. Results:The relative expression of microRNA-150 in the atrial tissue of the atrial fibrillation group was lower than that in the control group (P<0.05).The expression of microRNA-150 in H9c2 cardiomyocytes of the microRNA-150 group was significantly higher than that in the negative control group and the blank control group (P<0.05).The levels of cMyb mRNA and protein in H9c2 cardiomyocytes of the microRNA-150 group were significantly lower than those in the negative control group and the blank control group (P<0.05).The level of collagen Ⅰ in H9c2 cardiomyocytes of the microRNA-150 group was significantly lower than that of the negative control group and the blank control group (P<0.05).The levels of MMP-9 and TGF-β1 in H9c2 cardiomyocytes in the microRNA-150 group were significantly lower than those in the negative control group and the blank control group (P<0.05).There were no significant difference in each indicator of H9c2 cardiomyocytes between the negative control group and the blank control group (P> 0.05). Conclusion:The expression of microRNA-150 in atrial tissue of patients with atrial fibrillation decreases. Increasing the expression of microRNA-150 in cardiomyocytes can decrease myocardial cell fibrosis through the target gene cMyb.

参考文献:

[1] PRYSTOWSKY E N,PADANILAM B J,FOGEL R I.Treatment of Atrial Fibrillation[J].JAMA,2015,314(3):278-288.
[2] BORIANI G,LAROCHE C,DIEMBERGER I,et al.Asymptomatic atrial fibrillation:clinical correlates,management,and outcomes in the EORP-AF Pilot General Registry[J].Am J Med,2015,128(5):509-518.
[3] YUAN C T,LI X X,CHENG Q J,et al.MiR-30a regulates the atrial fibrillation-induced myocardial fibrosis by targeting snail 1[J].Int J Clin Exp Pathol,2015,8(12):15527-15536.
[4] RANGANATHAN P,JAYAKUMAR C,TANG Y,et al.microRNA-150 deletion in mice protects kidney from myocardial infarction-induced acute kidney injury[J].Am J Physiol Renal Physiol,2015,309(6):F551-558.
[5] MOHR A M,MOTT J L.Overview of microRNA biology[J].Semin Liver Dis,2015,35(1):3-11.
[6] HAYES J,PERUZZI P P,LAWLER S.MicroRNAs in cancer:biomarkers,functions and therapy[J].Trends Mol Med,2014,20(8):460-469.
[7] SUN J S,ZHANG X L,YANG Y J,et al.Hypoxia promotes C-X-C chemokine receptor type 4 expression through microRNA-150 in pancreatic cancer cells[J].Oncol Lett,2015,10(2):835-840.
[8] 杨雅静,李利廷,于卫芳,等.结直肠癌组织中miR-150表达及其对癌细胞增殖的影响[J].山东医药,2016,56(2):5-7.
[9] YIN Q W,SUN X F,YANG G T,et al.Increased expression of microRNA-150 is associated with poor prognosis in non-small cell lung cancer[J].Int J Clin Exp Pathol,2015,8(1):842-846.
[10] 于卫芳,翟从劼,樊智彬,等.miR-150和miR-134在结直肠癌及腺瘤中的表达[J].中国普通外科杂志,2014,23(10):1349-1354.
[11] WANG F,REN X,ZHANG X.Role of microRNA-150 in solid tumors[J].Oncol Lett,2015,10(1):11-16.
[12] LI X,CHEN L,WANG W,et al.microRNA-150 inhibits cell invasion and migration and is downregulated in human osteosarcoma[J].Cytogenet Genome Res,2015,146(2):124-135.
[13] DENG P,CHEN L,LIU Z,et al.microRNA-150 inhibits the activation of cardiac fibroblasts by regulating c-Myb[J].Cell Physiol Biochem,2016,38(6):2103-2122.
[14] 崔云霞,毕慧梅,闫俊霞,等.microRNA-150在糖尿病心肌纤维化中的变化及对胶原Ⅰ的影响[J].中国卫生检验杂志,2012,22(2):208-210.
[15] 周小翠,汪涛,李恩.miR-150通过靶基因c-Myb改善心肌梗死后心肌纤维化[J].实用医学杂志,2017,33(7):1078-1082.
[16] HEINDRYCKX F,BINET F,PONTICOS M,et al.Endoplasmic reticulum stress enhances fibrosis through IRE1α-mediated degradation of miR-150 and XBP-1 splicing[J].EMBO Mol Med,2016,8(7):729-744.
[17] SUI X,WEI H,WANG D.Novel mechanism of cardiac protection by valsartan:synergetic roles of TGF-β1 and HIF-1α in Ang Ⅱ-mediated fibrosis after myocardial infarction[J].J Cell Mol Med,2015,19(8):1773-1782.
[18] LI Z,BI X,WANG M,et al.Inhibition of farnesyl pyrophosphate synthase prevents angiotensin Ⅱ-induced cardiac fibrosis in vitro[J].Clin Exp Immunol,2014,176(3):429-437.
[19] 王爱波.急性心肌梗死并发心房颤动的相关因素及近期预后分析[J].现代医学,2016,44(8):1104-1106.
[20] WANG X,LV H,GU Y,et al.Protective effect of lycopene on cardiac function and myocardial fibrosis after acute myocardial infarction in rats via the modulation of p38 and MMP-9[J].J Mol Histol,2014,5(1):113-120.

服务与反馈:
文章下载】【发表评论】【查看评论】【加入收藏
提示:您还未登录,请登录!点此登录
您是第 465728 位访问者


copyright ©《东南大学学报(医学版)》编辑部
联系电话:025-83272481 83272483
电子邮件:
bjb@pub.seu.edu.cn

本系统由北京博渊星辰网络科技有限公司设计开发 技术支持电话:010-63361626

苏ICP备09058364