Identification of potentially relevant genes for myocardial infarction using RNA sequencing data analysis

Abstract

Myocardial infarction (MI) is a heart disease with high morbidity and mortality rates, thus it is critical to identify genes that serve roles during its pathogenesis. The objective of the present study was to identify potentially relevant genes during the progression of the disease. Blood samples from patients with MI and normal controls (n=3/group) were obtained, the RNA was extracted and cDNA libraries were established. RNA sequencing (RNA-seq) was performed on a HiSeq 2500 platform and fragments per kilobase of exon per million fragments mapped was utilized to calculate the gene expression value following preprocessing of the RNA-seq data. Electronic validation of several identified differentially expressed genes (DEGs) was performed on a Gene Expression Omnibus (GEO) dataset GSE59867 (390 cases and 46 healthy controls). Functional enrichment and protein-protein interaction network analysis was conducted for DEGs. A total of 977 DEGs, including 817 upregulated and 160 downregulated genes were identified in patients with MI. These DEGs were significantly enriched for ‘positive regulation of the immune system process,’ ‘inflammatory response,’ ‘regulation of I-kappaB-kinase/NF-kappaB signaling’ and ‘TNF signaling pathway’. A protein-protein interaction network of the top 40 DEGs was used to identify high degree genes, including interferon induced protein with tetratricopeptide repeats 3 (IFIT3), MX dynamin like GTPase 1 (MX1), major histocompatibility complex, class II, DQ α1 (HLA-DQA1), RAR related orphan receptor A (RORA), prostaglandin D2 synthase (PTGDS), cysteine rich protein 2 (CRIP2), collagen type VI α 2 chain (COL6A2) and S100 calcium binding protein P (S100P). The results of validation in the GEO dataset were consistent with the sequencing analysis. A total of eight genes, including IFIT3, MX1, HLA-DQA1, RORA, PTGDS, CRIP2, COL6A2 and S100P may therefore be considered as potentially relevant genes in the pathology of MI.

lncRNA FGD5 antisense RNA 1 upregulates RORA to suppress hypoxic injury of human cardiomyocyte cells by inhibiting oxidative stress and apoptosis via miR‑195

“…The present study confirmed rora downregulation in the serum of patients with aMi and hypoxia-treated ac16 cells, indicating a potential role of rora in myocardial anoxia. Moreover, rora, along with seven other genes, has been identified as a key gene in myocardial infarction, according to rna sequencing data (41). He et al (20) identified the protective role of RORA in myocardial i/r injury, and proposed that rora was downregulated in a mouse heart following I/R.…”

Downregulation of interferon-induced protein with tetratricopeptide repeats 3 relieves the inflammatory response and myocardial fibrosis of mice with myocardial infarction and improves their cardiac function

“…Moreover, a study based on transcriptional profile analysis showed that upregulated IFIT3 expression was observed in human ischemic cardiac hypertrophy and MI animal models [ 11 ]. Furthermore, RNA sequencing using blood samples from patients with MI and normal controls showed that IFIT3 was upregulated in the MI patients and might be potentially relevant to the pathology of MI [ 12 ]. However, the function of IFIT3 in MI has not been reported yet.…”

Identification of Biomarkers Related to Immune Cell Infiltration with Gene Coexpression Network in Myocardial Infarction

“…It can lead to loss of cardiomyocytes, left ventricular remodeling, decreased cardiac function, and potentially heart failure. MI is associated with a variety of factors, including gender, age, smoking, hypertension, and diabetes complications [2]. Microarray analysis is a widely used strategy for detecting novel biomarkers for diagnosis, prediction of disease severity, and identification of new drug targets [3].…”