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Braz J Med Biol Res. 2016 Oct 10;49(10):e4897. doi: 10.1590/1414-431X20164897.

Analyzing gene expression profiles in dilated cardiomyopathy via bioinformatics methods.

Author information

1
Emergency Department, The Second Affiliated Hospital of Xi'an, Jiaotong University, Xi'an, China.
2
Department of Emergency Medicine, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
3
Medical Department, The First Affiliated Hospital of Harbin Medical University, Harbin, China.

Abstract

Dilated cardiomyopathy (DCM) is characterized by ventricular dilatation, and it is a common cause of heart failure and cardiac transplantation. This study aimed to explore potential DCM-related genes and their underlying regulatory mechanism using methods of bioinformatics. The gene expression profiles of GSE3586 were downloaded from Gene Expression Omnibus database, including 15 normal samples and 13 DCM samples. The differentially expressed genes (DEGs) were identified between normal and DCM samples using Limma package in R language. Pathway enrichment analysis of DEGs was then performed. Meanwhile, the potential transcription factors (TFs) and microRNAs (miRNAs) of these DEGs were predicted based on their binding sequences. In addition, DEGs were mapped to the cMap database to find the potential small molecule drugs. A total of 4777 genes were identified as DEGs by comparing gene expression profiles between DCM and control samples. DEGs were significantly enriched in 26 pathways, such as lymphocyte TarBase pathway and androgen receptor signaling pathway. Furthermore, potential TFs (SP1, LEF1, and NFAT) were identified, as well as potential miRNAs (miR-9, miR-200 family, and miR-30 family). Additionally, small molecules like isoflupredone and trihexyphenidyl were found to be potential therapeutic drugs for DCM. The identified DEGs (PRSS12 and FOXG1), potential TFs, as well as potential miRNAs, might be involved in DCM.

PMID:
27737314
PMCID:
PMC5064772
DOI:
10.1590/1414-431X20164897
[Indexed for MEDLINE]
Free PMC Article

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