LncRNA and mRNA interaction study based on transcriptome profiles reveals potential core genes in the pathogenesis of human thoracic aortic dissection.
LncRNA and mRNA interaction study based on transcriptome profiles reveals potential core genes in the pathogenesis of human thoracic aortic dissection.
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DOI：
10.3892/mmr.2018.9308
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发表时间：
2018-09
影响因子：
3.4
通讯作者：
Li D
中科院分区：
文献类型：
--
作者：
Li Y;Yang N;Zhou X;Bian X;Qiu G;Zhang M;Lin H;Li D
本研究的目的是通过分析人胸主动脉夹层（thoracic aortic dissection，CHD）与正常胸主动脉（normal thoracic aortic aorta，NTA）之间的长链非编码（long non-coding，lnc）RNAs基因芯片表达谱，确定CHD发病机制中潜在的核心基因。采用lncRNA芯片技术，分析正常对照组（n=6）和正常对照组（n=6）主动脉组织中lncRNA的差异表达。基因本体论（GO），通路和网络分析用于进一步研究候选lncRNA和mRNA。通过逆转录-定量聚合酶链反应（RT-qPCR）验证差异表达的lncRNA和mRNA。本研究共鉴定出765条lncRNA和619条mRNA在NTA和NTA之间存在差异表达（倍数变化>2.0，P<0.01）。GO分析表明，差异上调的lncRNA与细胞分化，稳态，细胞生长和血管生成有关。京都基因百科全书和基因组通路分析表明，差异下调的lncRNA主要与致瘤性右心室心肌病、肥厚型心肌病和扩张型心肌病有关。为了减少用于进一步研究的lncRNA，并富集那些可能参与转录的lncRNA，选择了总共16个具有显著表达（倍数变化>4，P<0.01）的候选lncRNA，其通过GO术语和科学文献与注释的蛋白质编码基因相关。然后，一组显著表达的lncRNA [嘌呤能受体P2 X7（P2 RX 7），缺氧诱导因子（HIF）-1A-AS 2，AX 746823，RP 11 - 69 I8.3和RP 11 - 536 K7.5）和相应的mRNA（P2 RX 7，细胞周期蛋白依赖性激酶抑制剂2B，HIF-1A，runt相关转录因子1，结缔组织生长因子和白细胞介素2受体α链]。本研究显示，lncRNA和mRNA在主动脉组织中的表达谱显着改变。这些结果可能提供重要的见解的发病机制，糖尿病。
The aim of the present study was to determine the potential core genes in the pathogenesis of human thoracic aortic dissection (TAD) by analyzing microarray profiles of long non-coding (lnc)-RNAs between TAD and normal thoracic aorta (NTA). The differentially expressed lncRNA profiles of the aorta tissues between TAD patients (TAD group, n=6) and age-matched donors with aortic diseases (NTA group, n=6) were analyzed by lncRNAs microarray. Gene ontology (GO), pathway and network analyses were used to further investigate candidate lncRNAs and mRNAs. Differentially expressed lncRNAs and mRNAs were validated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). In total, the present study identified 765 lncRNAs and 619 mRNAs with differential expression between TAD and NTA (fold change >2.0, P<0.01). GO analysis demonstrated that the differentially upregulated lncRNAs are associated with cell differentiation, homeostasis, cell growth and angiogenesis. Kyoto Encyclopedia of Gene and Genomes pathway analysis demonstrated that the differentially downregulated lncRNAs are mainly associated with arrhythmogenic right ventricular cardiomyopathy, hypertrophic cardiomyopathy and dilated cardiomyopathy. To reduce the lncRNAs for further investigation and to enrich those potentially involved in TAD, a total of 16 candidate lncRNAs with a significant expression (fold change >4, P<0.01) were selected, that were associated with an annotated protein-coding gene through the GO term and scientific literatures. Then a set of significantly expressed lncRNAs [purinergic receptor P2X7 (P2RX7), hypoxia inducing factor (HIF)-1A-AS2, AX746823, RP11-69I8.3 and RP11-536K7.5) and the corresponding mRNAs (P2RX7, cyclin dependent kinase inhibitor 2B, HIF-1A, runt-related transcription factor 1, connective tissue growth factor and interleukin 2 receptor a chain] were confirmed using RT-qPCR. The present study revealed that the expression profiles of lncRNAs and mRNAs in aorta tissues from TAD were significantly altered. These results may provide important insights into the pathogenesis of TAD disease.
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影响因子：
20.1
作者：
Leung A;Trac C;Jin W;Lanting L;Akbany A;Sætrom P;Schones DE;Natarajan R
通讯作者：
Natarajan R
DOI：
10.1042/cs20120479
发表时间：
2013-08
期刊：
Clinical science (London, England : 1979)
影响因子：
--
作者：
Chiao CW;da Silva-Santos JE;Giachini FR;Tostes RC;Su MJ;Webb RC
通讯作者：
Webb RC
影响因子：
5.4
作者：
Kornienko AE;Guenzl PM;Barlow DP;Pauler FM
通讯作者：
Pauler FM
BRG1在胸主动脉瘤中表达增加并在体外通过长非编码RNA HIF1A-AS1调节血管平滑肌细胞的增殖和凋亡
影响因子：
3.4
作者：
Wang, Shuwei;Zhang, Xiwu;Xu, Zhiyun
通讯作者：
Xu, Zhiyun
DOI：
10.1161/atvbaha.112.300399
发表时间：
2013-01
期刊：
Arteriosclerosis, thrombosis, and vascular biology
影响因子：
--
作者：
Leeper NJ;Raiesdana A;Kojima Y;Kundu RK;Cheng H;Maegdefessel L;Toh R;Ahn GO;Ali ZA;Anderson DR;Miller CL;Roberts SC;Spin JM;de Almeida PE;Wu JC;Xu B;Cheng K;Quertermous M;Kundu S;Kortekaas KE;Berzin E;Downing KP;Dalman RL;Tsao PS;Schadt EE;Owens GK;Quertermous T
通讯作者：
Quertermous T