Association of interleukin-17 and phagosome with healing after acute myocardial infarction

Acute myocardial infarction is one of the main causes of mortality in the worldwide. The aim of the present study is to predict the Association of interleukin (IL)-17 and phagosome with acute myocardial infarction.

Methods and Materials:

Microarray data were extracted from National Center for Biotechnology Information (NCBI) and then analyzed by GEO2R and R softwares. The functional analysis of up/down regulation of genes were performed using DAVID and Enrichr data bases.

In this study, expression of 208 genes were lower in patients group compared to the controls (Log2FC<-1). In patients’ group, PAQR8, CCR2, CCR5, and ZNF137P genes significantly had lower expression. Although 528 gens, especially NR4A2, GABARAPL1, THBD, NFIL3, and MAFB significantly had more expression compared to the controls (Log2FC>+1). KEGG analysis on gens that increase expression showed that signaling pathways of IL-17 and phagosome are two pathways in patients with acute myocardial infarction.

According to our finding, after acute myocardial infarction, inflammatory pathway like IL-17 signaling recruiting matrix metalloproteinase 9 as a protein involve in repairing acute myocardial infarction damages. Also, the phagosome activity by major histocompatibility complex class-II (MHC-II) and CD36 signaling pathways, may be played a role in accelerating healing after acute myocardial infarction damages.