Analyzing gene expression profiles with preliminary validations in cardiac hypertrophy induced by pressure overload

被引:8
作者
Gao, Jing [1 ,2 ]
Li, Yuhong [2 ]
Wang, Tongmei [3 ]
Shi, Zhuo [4 ]
Zhang, Yiqi [3 ]
Liu, Shuang [1 ]
Wen, Pushuai [3 ]
Ma, Chunyan [1 ]
机构
[1] China Med Univ, Hosp 1, Dept Cardiovasc Ultrasound, Shenyang 110001, Liaoning, Peoples R China
[2] Jinzhou Med Univ, Dept Ultrasonog, Affiliated Hosp 1, Jinzhou 121001, Peoples R China
[3] Jinzhou Med Univ, Dept Pathophysiol, Jinzhou 121001, Peoples R China
[4] Jinzhou Med Univ, Dept Anat, Jinzhou 121001, Peoples R China
基金
中国国家自然科学基金;
关键词
cardiac hypertrophy; differentially expressed genes; pathway enrichment analysis; isoprenaline; functional enrichment analysis; JUN NH2-TERMINAL KINASE; FOCAL ADHESION KINASE; GROWTH-FACTOR; HEART-FAILURE; ACTIVATION; RECEPTOR; FIBROSIS; VOLUME; HYPERTENSION; STIMULATION;
D O I
10.1139/cjpp-2017-0585
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
The aim of this study was to identify the key genes involved in the cardiac hypertrophy (CH) induced by pressure overload. mRNA microarray data sets GSE5500 and GSE18801 were downloaded from the Gene Expression Omnibus database, and differentially expressed genes (DEGs) were screened using the Limma package; then, functional and pathway enrichment analysis were performed for common DEGs using the Database for Annotation, Visualization and Integrated Discovery database. Furthermore, the top DEGs were further validated using quantitative PCR in the hypertrophic heart tissue induced by isoprenaline. A total of 113 common DEGs with absolute fold change > 0.5, including 60 significantly upregulated DEGs and 53 down-regulated DEGs, were obtained. Gene ontology term enrichment analysis suggested that common upregulated DEG were mainly enriched in neutrophil chemotaxis, extracellular fibril organization, and cell proliferation; and the common downregulated genes were significantly enriched in ion transport, endoplasmic reticulum, and dendritic spine. Kyoto Encyclopedia of Genes and Genomes pathway analysis found that the common DEGs were mainly enriched in extracellular matrix receptor interaction, phagosome, and focal adhesion. Additionally, the expression of Mfap4, Ltbp2, Aspn, Serpina3n, and Cnksr1 were upregulated in the model of CH, while the expression of Anp32a was downregulated. The current study identified the key deregulated genes and pathways involved in the CH, which could shed new light to understand the mechanism of CH.
引用
收藏
页码:701 / 709
页数:9
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