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|本期目录/Table of Contents|

血管紧张素 II通过增加miR-21表达促进心脏成纤维细胞胶原合成

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2017年第1期
页码:
40-043
栏目:
基础研究
出版日期:
2016-10-05

文章信息/Info

Title:
Angiotensin II promotes collagen synthesis in cardiac fibroblast via miR-21
作者:
周宇航12周宇晖3杨国栋2柏丹娜24
(1.昆明市第三人民医院心内科,云南 昆明 650041;
2.第四军医大学生物化学与分子生物学教研室,陕西 西安 710032;
3.曲靖市第一人民医院肾内科,云南 曲靖 655000;
4.解放军第三二三医院心内科,陕西 西安 710054)
Author(s):
ZHOU Yu-hang12 ZHOU Yu-hui3 YANG Guo-dong2 BAI Dan-na24
(1.Department of Cardiology, Third People’s Hospital, Kunming 650041, Yunnan, China;
2.Department of Biochemistry and Molecular Biology, Fourth Military Medical University, Xi’an 710032, Shaanxi, China;
3.Department of Nephrology, First People’s
关键词:
血管紧张素II胶原微小RNA-21心脏成纤维细胞信号转导
Keywords:
angiotensin II collagen microRNA-21 cardiac fibroblasts signal transduction
分类号:
R972
DOI:
-
文献标识码:
A
摘要:
目的 探讨血管紧张素II(AngII)促进心脏成纤维细胞胶原合成的分子机制,初步分析miR-21在其中发挥的作用。方法 使用SD大鼠心脏组织分离培养原代成纤维细胞;分别使用0、0.1、0.2和0.4 μmol/L的AngII刺激细胞36 h,qRT-PCR检测胶原(Col1a1和Col3a1)和miR-21的表达变化;使用miR-21抑制物(miR-21 inhibitor)转染细胞,AngII刺激后,qRT-PCR检测Col1a1和Col3a1的表达。结果 镜下观察和标志物分子检测表明心脏成纤维细胞培养成功。在AngII刺激下,Col1a1、Col3a1和miR-21均呈剂量依赖性表达增加(P<0.05)。使用miR-21抑制物能显著降低Ang II刺激下Col1a1和Col3a1的表达升高(P<0.05)。结论 AngII能增加心脏成纤维细胞的胶原合成,其相关机制可能部分通过miR-21相关信号来介导。
Abstract:
AIM To explore the role of angiotensin II (AngII) in the collagen synthesis of cardiac fibroblasts and the putative involvement of miR-21. METHODSPrimary cardiac fibroblast cells were isolated from Sprague Dawley rats and the cells were treated with 0, 0.1, 0.2 and 0.4 μmol/L AngII for 36 h. Expressions of Col1a1, Col3a1 and miR21 were analyzed by qRT-PCR. MiR-21 was knocked down by transfected miR-21 inhibitor into cardiac fibroblast cells. RESULTSCardiac fibroblast cells were successfully isolated and cultured as seen morphologically under the microscope and expression of the markers. Upon AngII treatment, expressions of Col1a1, Col3a1 and miR21 increased in a dose-dependent manner. miR21 inhibitor markedly blocked the induction of Col1a1 and Col3a1 by AngII. CONCLUSIONAngII induces collagen synthesis in which induction of miR-21 might be essential.

参考文献/References

[1]Brown RD,Ambler SK,Mitchell MD,et al.The cardiac fibroblast:therapeutic target in myocardial remodeling and failure[J].Annu Rev Pharmacol Toxicol,2005,45:657-687.
[2]Porter KE,Turner NA.Cardiac fibroblasts:at the heart of myocardial remodeling[J].Pharmacol Ther,2009,123(2):255-278.
[3]Iwata M,Cowling RT,Yeo SJ,et al.Targeting the ACE2-Ang-(1-7)pathway in cardiac fibroblasts to treat cardiac remodeling and heart failure[J]. J Mol Cell Cardiol,2011,51(4):542-547.
[4]Banerjee I,Yekkala K,Borg TK,et al.Dynamic interactions between myocytes,fibroblasts, and extracellular matrix[J].Ann N Y Acad Sci,2006,1080:76-84.
[5]Romaine SP,Tomaszewski M,Condorelli G,et al.MicroRNAs in cardiovascular disease:an introduction for clinicians[J].Heart,2015,101(12):921-928.
[6]Lawrie CH.MicroRNAs and lymphomagenesis:a functional review[J].Br J Haematol,2013,160(5):571-581.
[7]Indolfi C,Curcio A.Stargazing microRNA maps a new miR-21 star for cardiac hypertrophy[J].J Clin Invest,2014,124(5):1896-1898.
[8]Liu S,Li W,Xu M,et al.Micro-RNA 21 Targets dual specific phosphatase 8 to promote collagen synthesis in high glucose-treated primary cardiac fibroblasts[J].Can J Cardiol,2014,30(12):1689-1699.
[9]Castoldi G,Di Gioia CR,Bombardi C,et al.MiR-133a regulates collagen 1A1:potential role of miR-133a in myocardial fibrosis in angiotensin II-dependent hypertension[J].J Cell physiol,2012,227(2):850-856.
[10]Dostal D,Glaser S,Baudino TA.Cardiac fibroblast physiology and pathology[J].Compr Physiol,2015,5(2):887-909.
[11]Deb A,Ubil E.Cardiac fibroblast in development and wound healing[J].J Mol Cell cardiol,2014,70:47-55.
[12]Roche P,Czubryt MP.Transcriptional control of collagen I gene expression[J].Cardiovasc Hematol Disord Drug Targets,2014,14(2):107-120.
[13]Cao Z,Cooper ME:Efficacy of renin-angiotensin system(RAS)blockers on cardiovascular and renal outcomes in patients with type 2 diabetes[J].Acta Diabetol,2012,49(4):243-254.
[14]Lindsay ME,Dietz HC.Lessons on the pathogenesis of aneurysm from heritable conditions[J].Nature,2011,473(7347):308-316.
[15]McKinney CA,Fattah C,Loughrey CM,et al.Angiotensin-(1-7)and angiotensin-(1-9):function in cardiac and vascular remodelling[J].Clin Sci,2014,126(12):815-827.
[16]Nishida M,Kitajima N,Saiki S,et al.Regulation of Angiotensin II receptor signaling by cysteine modification of NF-kappaB[J].Nitric oxide,2011,25(2):112-117.
[17]Rosenkranz S.TGF-beta1 and angiotensin networking in cardiac remodeling[J].Cardiovasc Res,2004,63(3):423-432.
[18]Thum T,Gross C,Fiedler J,et al.MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts[J].Nature,2008,456(7224):980-984.
[19]Cheng Y,Ji R,Yue J,et al.MicroRNAs are aberrantly expressed in hypertrophic heart:do they play a role in cardiac hypertrophy?[J].Am J Pathol,2007,170(6):1831-1840.
[20]Adam O,Lohfelm B,Thum T,et al.Role of miR-21 in the pathogenesis of atrial fibrosis[J].Basic Res Cardiol,2012,107(5):278.

备注/Memo

备注/Memo:
收稿日期:2015-08-26.基金项目:陕西省自然科学基金项目资助(2014JM4182)
通讯作者:柏丹娜,主治医师,主要从事心脏纤维化分子机制研究 Email:danabai@163.com
作者简介:周宇航,硕士生 Email:82533004@qq.com
更新日期/Last Update: 2016-10-09