Correlation of miR-24-3p and miR-595 expression with CCL3, CCL4, IL1-beta, TNFalphaIP3, and NF-kappaBIalpha genes in PBMCs of patients with coronary artery disease.

Inflammation has been well recognized to play an important role in developing coronary artery disease (CAD). By regulating essential genes in this pathway post-transcriptionally, MicroRNAs (miRNAs) may help or hinder the development of atherosclerotic lesions. The aim of this study was to investigate the expression of miR-24-3p, miR-595, CCL3, CCL4, IL-1ß, TNFαIP3, and NF-κBIα in the peripheral blood mononuclear cells (PBMCs) of CAD and control groups and to examine whether any correlation exists between the expression of miRs and genes in CAD group. A total of 168 subjects (84 CAD subjects and 84 control subjects) were examined in this research. Expression levels of miR-24-3p, miR-595, CCL3, CCL4, IL-1ß, TNFαIP3, and NF-κBIα in PBMCs were measured using the real-time PCR technique. A comparison of the CAD group with the control group indicated significantly increased expression levels of CCL3, CCL4, and IL-1ß (Fold Change (FC)=4, P=0.009; FC=2.9, P=0.01; FC=1.8, P=0.019, respectively) and remarkably reduced expression levels of TNFαIP3 and NF-κBIα (FC=-1.4, P=0.03 and FC=-5.9, P=0.001, respectively). Moreover, the expression levels of miR-24-3p downregulated (FC=-2.5, P=0.005) and miR-595 upregulated (FC=1.9, P=0.009) in the CAD group. There was a statistical correlation between the number of clogged arteries with expression levels of miR-24-3p, miR-595, CCL3, CCL4, IL-1ß, TNFαIP3, and NF-κBIα in the CAD group. Also, there was a statistical correlation between expression levels of miR-24-3p and miR-595 with CCL3, CCL4, IL-1ß, TNFαIP3, and NF-κBIα gene expression in the CAD group. In CAD patients, decreased expression of miR-24-3p and increased expression of miR-595 may aid the progression of atherosclerotic plaques by regulating CCL3, CCL4, IL-1ß, TNFαIP3, and NF-κBIα gene expression.

The Serum Levels of IL-36 in Patients with Coronary Artery Disease and Their Correlation with the Serum Levels of IL-32, IL-6, TNF-α, and Oxidative Stress.

INTRODUCTION: Atherosclerosis is a chronic inflammatory process maintained during all stages of the disease by several proinflammatory mediators, such as cytokines and chemokines. Interleukin (IL)-36 cytokines are proinflammatory and have an essential role in innate and adaptive immunity, but the role of IL-36 has not been determined in coronary artery disease (CAD). This study aimed to measure the serum levels of IL-36 in patients with CAD and their association with the serum levels of tumor necrosis factor (TNF)-α, IL-6, and IL-32 and also investigate their correlation with the serum levels of malondialdehyde (MDA) and ferric reducing antioxidant power (FRAP). METHODS: A total of 168 subjects (84 CAD and 84 control subjects) were examined in this research. The total serum levels of IL-36 were measured using the enzyme-linked immunosorbent assay (ELISA). Also, some oxidative stress parameters were evaluated by FRAP and MDA assays in the serum. RESULTS: The serum levels of IL-36 and MDA were significantly higher, and FRAP was significantly lower in the CAD group compared to the controls. Furthermore, the serum levels of IL-36, MDA, and FRAP significantly correlated with the CAD group's cardiac arterial stenosis. Also, the serum levels of IL-36 had a positive and significant correlation with the serum levels of TNF-α, IL-6, IL-32, and biochemical parameters in the CAD group. CONCLUSION: Higher serum levels of IL-36 and its association with the serum levels of TNF-α, IL-32, and IL-6 may play a key role in the pathogenesis of CAD, leading to an increased risk of clogged arteries and oxidative stress.

Serum levels of IL-37 and correlation with inflammatory cytokines and clinical outcomes in patients with coronary artery disease.

Coronary artery disease (CAD) due to atherosclerosis is one of the important reasons for death worldwide. Recent evidence has suggested the essential role of inflammation in the progression of atherosclerosis. Interleukin (IL)-37 is a critical anti-inflammatory member of the IL-1 family which regulates the inflammatory processes. The aim of this study was to compare the serum levels of IL-37 in patients with CAD compared with the control group and its correlation with oxidative stress, cholesterol homeostasis, and inflammation in patients with CAD. A total of 42 patients with CAD and 42 sex-matched and age- matched controls who underwent coronary angiography were included in this study. The serum levels of IL-37 were evaluated via ELISA. Serum levels of biochemical risk factors were determined by enzymatic methods. Serum levels of IL-37 in the CAD group subjects were significantly lower than in the control group and IL-37 was significantly increased in men with CAD than in women with CAD. IL-37 significantly had an inverse correlation with IL-6, tumor necrosis factor-α, IL-32, high-sensitivity C reactive protein, oxidized low-density lipoprotein, and malondialdehyde. Also, IL-37 had a significantly positive correlation with ferric-reducing antioxidant power (FRAP) assay. In addition, IL-37 has positively correlated with ATP-binding cassette transporter A1 and G1 gene expression in peripheral blood mononuclear cells and serum levels of the FRAP. A receiver operating characteristic test displayed that IL-37 level ratios were a relatively significant CAD predictor. Our results indicated that decreased serum levels of IL-37 in patients with CAD and its relationship with inflammatory cytokines and reverse cholesterol transport genes are more likely to be associated in the inflammatory process with disease pathology.