Integration of gene expression profile data of human epicardial adipose tissue from coronary artery disease to verification of hub genes and pathways

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Abstract

Background. This study aim to identify the core pathogenic genes and explore the potential molecular mechanisms of human coronary artery disease (CAD). Methodology. Two gene profiles of epicardial adipose tissue from CAD patients including GSE 18612 and GSE 64554 were downloaded and integrated by R software packages. All the coexpression of deferentially expressed genes (DEGs) were picked out and analyzed by DAVID online bioinformatic tools. In addition, the DEGs were totally typed into protein-protein interaction (PPI) networks to get the interaction data among all coexpression genes. Pictures were drawn by cytoscape software with the PPI networks data. CytoHubba were used to predict the hub genes by degree analysis. Finally all the top 10 hub genes and prediction genes in Molecular complex detection were analyzed by Gene ontology and Kyoto encyclopedia of genes and genomes pathway analysis. qRT-PCR were used to identified all the 10 hub genes. Results. The top 10 hub genes calculated by the degree method were AKT1, MYC, EGFR, ACTB, CDC42, IGF1, FGF2, CXCR4, MMP2 and LYN, which relevant with the focal adhesion pathway. Module analysis revealed that the focal adhesion was also acted an important role in CAD, which was consistence with cytoHubba. All the top 10 hub genes were verified by qRT-PCR which presented that AKT1, EGFR, CDC42, FGF2, and MMP2 were significantly decreased in epicardial adipose tissue of CAD samples (p<0.05) and MYC, ACTB, IGF1, CXCR4, and LYN were significantly increased (p<0.05). Conclusions. These candidate genes could be used as potential diagnostic biomarkers and therapeutic targets of CAD.

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Wang, W., Liu, Q., Wang, Y., Piao, H., Li, B., Zhu, Z., … Liu, K. (2019). Integration of gene expression profile data of human epicardial adipose tissue from coronary artery disease to verification of hub genes and pathways. BioMed Research International, 2019. https://doi.org/10.1155/2019/8567306

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