我们的网站为什么显示成这样?

可能因为您的浏览器不支持样式,您可以更新您的浏览器到最新版本,以获取对此功能的支持,访问下面的网站,获取关于浏览器的信息:

|本期目录/Table of Contents|

血浆miRNA在先天性心脏病继发肺动脉高压的差异表达

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2018年第4期
页码:
442-445
栏目:
临床研究
出版日期:
2018-04-25

文章信息/Info

Title:
Differential expression of plasma miRNA in patients with congenital heart disease and pulmonary arterial hypertension
作者:
郭建洲王志伟马琰琰
(深圳市孙逸仙心血管医院外三科,广东 深圳 518020)
Author(s):
GUO Jian-zhou WANG Zhi-wei MA Yan-yan
(Department of Surgery, The sun yat-sen cardiovascular hospital, Shenzhen 518020, Guangdong, China)
关键词:
心脏病先天性肺动脉高压微小核糖核酸表达谱相关性
Keywords:
congenital heart disease pulmonary hypertension miRNA expression profile correlation
分类号:
R541.1
DOI:
-
文献标识码:
A
摘要:
目的 探究先天性心脏病继发肺动脉高压(PAH)患者血浆中miRNA表达谱的差异,从而探究其与PAH的相关性。方法 先天性心脏病患者80例,根据肺动脉压力进行分组:肺动脉压正常者22例(无PAH组);轻、中度PAH者37例(轻中度PAH组);重度PAH者21例(重度PAH组)。另外选取门诊体检的志愿者20例作为对照组。采用定量聚合酶链反应(PCR)分析对比各组患者血浆miR-18a、miR-27b、miR-130a和miR-204的表达差异。分析miRNA表达水平与肺动脉压力的相关性。结果 与对照组相比,无PAH组、轻中度PAH组、重度PAH组患者miR-18a、miR-27b和miR-130a表达水平上调,miR-204的表达水平下调,差异有统计学意义(P<0.05);与无PAH组相比,轻中度PAH组、重度PAH组患者miR-18a、miR-27b和miR-130a表达水平上调,miR-204的表达水平下调,差异有统计学意义(P<0.05);与轻中度PAH组相比,重度PAH组患者miR-18a、miR-27b和miR-130a表达水平上调,miR-204的表达水平下调,差异有统计学意义(P<0.05)。Spearman线性相关分析显示血浆miR-18a、miR-27b和miR-130a表达水平与PAH呈正相关(r=0.845,r=0.912,r=0.933,P<0.05);血浆miR-204的表达水平与PAH呈负相关(r=-0.629,P<0.05)。结论 miRNA在先天性心脏病继发PAH患者血浆中存在差异表达,miRNA的表达水平与肺动脉压力具有相关性。
Abstract:
AIM To investigate the difference of plasma miRNA expression in patients with congenital heart disease with pulmonary arterial hypertension, and to explore the correlation between expressions of PAH and plasma miRNA. METHODS 80 patients with congenital heart disease were admitted in Department of Cardiology of our hospital from February 2015 to June 2017, and were divided into three groups according to pulmonary artery pressure: 22 cases of pulmonary arterial pressure in the normal subjects (no PAH group); 37 cases of mild and moderate pulmonary hypertension (the mild and moderate PAH group); 21 cases of severe pulmonary hypertension (the severe PAH group). In addition, 20 volunteers were selected as the control group. Quantitative polymerase chain reaction (QPCR) was used to compare expression levels of plasma miR-18a, miR-27b, miR-130a and miR-204 in each group, in order to analyze the correlation between miRNA expression level and pulmonary arterial pressure. RESULTS Compared with the control group, expression levels of miR-18a, miR-27b, C group, miR-130a in the three groups increased, expression level of miR-204 decreased, and these difference were statistically significant (P<0.05); compared with the no PAH group, expression levels of miR-18a, miR-27b, miR-130a in the mild and moderate PAH group and severe PAH group increased, expression level of miR-204 was down regulated, and these difference were statistically significant (P<0.05); compared with the mild and moderate PAH group, the expression levels of miR-18a miR-27b, miR-130a in the severe PAH group increased, expression level of miR-204 decreased, and the differences were statistically significant (P<0.05). Spearman correlation analysis showed that the expression levels of plasma miR-18a, miR-27b, miR-130a were positively correlated with pulmonary arterial hypertension (r=0.845, r=0.912, r=0.933, P<0.05); expression level of plasma miR-204 was negatively correlated with pulmonary arterial hypertension (r=-0.629, P<0.05). CONCLUSION miRNA expression is different in plasma of patients with PAH secondary to congenital heart disease. The expression level of miRNA is associated with pulmonary arterial pressure.

参考文献/References

[1]卢荣鑫,钟前进.左向右分流型肺动脉高压大鼠肺组织中microRNA的表达谱及初步分析[J].第三军医大学学报,2012,34(6):504-507.

[2]Meoli DF,White RJ.Endothelin-1 induces pulmonary but not aorticsmooth muscle cell migration by activating ERK1/2 MAP kinase[J].Can J Physiol Pharmacol,2010,88(8):830-839.

[3]Thum T,Galuppo P,Haverich A.MicroRNAs in the human heart:a clue to fetal gene reprogramming in heart failure[J].Circulation,2011,116(3):258-267.

[4]Jeffery TK,Morrell NW.Molecular and cellular basis of pulmonary vascular remodeling in pulmonary hypertension[J].Prog Cardiovasc Dis,2012,45(3):173-202.

[5]中华医学会心血管病学分会,中华心血管病杂志编辑委员会.肺动脉高压筛查诊断与治疗专家共识[J].中华心血管病杂志,2007,35(11):979-981.[J].岳天霞,袁 杰.先天性心脏病相关肺动脉高压患者的管理[J].心脏杂志,2013,25(1):116-119.

[7]陈伟丹,花中东,杨克明,等.microRNA在先天性心脏病继发性肺动脉高压肺组织内变化的实验研究[J].中国细胞生物学学报,2010,32(4):601-605.

[8]Fan F,Sun A,Zhao H,et al.MicroRNA-34a promotes cardiomyocyte apoptosis post myocardial infarction through don-regulating aldehyde dehydrogenase2[J].Curr Pharm Des,2013,19(27):4865-4873.

[9]Wagner J,Riwanto M,Besler C,et al.Characterization of levels and cellulartransfer of circulating lipoprotein-bound microRNAs[J].Arterioscler Thromb Vasc Biol,2013,33(6):1392-1400.

[10]Liebetrau C,Mollmann H,Dorr O,et al.Release kinetics of circulating muscle-enriched microRNAs in patients undergoing transcoronary ablation of septal hypertrophy[J].J Am Coll Cardiol,2013,62(11):992-998.

[11]Schulze-Neick I,Gilbert N,Ewert R,et al.Adult patients with congenital heart disease and pulmonary arterial hypertension. first open prospective multicenter study of bosentan therapy[J].Am Heart J,2005,150(4):716.

[12]Sabatel C,Malvaux L,Bovy N,et al.MicroRNA-27b exhibits antiangiogenic function by targeting RhoB expression in endothelial cells[J].PLoS One,2011,6(2):e16979.

[13]Vickers KC,PaImisano BT,Shoucri BM,et al.MicroRNAs are transported in plasma and delivered to recipient cells by high-density lipoproteins[J].Nat Cell Biol,2011,13(1):42-33.

备注/Memo

备注/Memo:
收稿日期:2017-09-25.作者简介:郭建洲,副主任医师 Email:guoxin997@sina.com
更新日期/Last Update: 1900-01-01