Abstract

Objectives This study aimed to investigate the association between inflammation-related microRNAs (miR-21, 146a, 155) and the plaque stability in coronary artery disease patients. Methods The expression of miR-21, 146a, and 155 was measured by real-time PCR in 310 consecutive patients. The level of hs-CRP, IL-6, and IL-8 was measured by ELISA. The plaque stability of coronary stenotic lesions was evaluated with intravascular ultrasound (IVUS). Results (1) The levels of hs-CRP, IL-6, and IL-8 were significantly increased in the UAP and AMI groups compared with the CPS group (P < 0.01). (2) The expression of miR-21 and miR-146a in peripheral blood mononuclear cells (PBMCs) and plasma was significantly higher in CAD patients compared with non-CAD patients, whereas the miR-155 expression in PBMCs and plasma was significantly lower in patients with CAD. (3) The miR-21 expression in PBMCs was higher in UAP and AMI groups compared with CPS group. The miR-146a expression in PBMCs was higher in SAP, UAP, and AMI groups than in CPS group. Although the level of miR-155 in PBMCs was lower in SAP, UAP, and AMI groups than in CPS group. The expression patterns of miR-21, miR-146a, and miR-155 in plasma were consistent with those of PBMCs. (4) The expressions of miR-21 and miR-146a in PBMCs and plasma were significantly higher in the vulnerable plaque group than those in stable plaque group. While miR-155 in PBMCs and plasma was significantly lower in vulnerable plaque group compared with stable plaque group. (5) The levels of miR-21 and miR-146a in PBMCs and plasma were significantly higher in soft plaque group than in fibrous plaque group and calcified plaque group. However, miR-155 in PBMCs and plasma was significantly lower in soft plaque group. Conclusions The expression of miR-21 and miR-146a are associated with the plaque stability in coronary stenotic lesions, whereas miR-155 expression is inversely associated with the plaque stability.

Highlights

  • At present, cardiovascular disease is the leading cause of death throughout the world. e mechanism of coronary artery disease is atherosclerosis (AS), which leads to coronary artery stenosis and myocardial ischemia

  • Our previous studies has con rmed that the expression of miR155 in peripheral blood mononuclear cells (PBMCs) and plasma was decreased in patients with coronary heart disease, and it was negatively correlated with the severity of the disease and coronary artery lesions assessed by Gensini score [12]

  • Basic Clinical Characteristics of Patients. ere were no significant differences in gender, age, and risk factors among patients with chest pain syndrome (CPS), stable angina pectoris (SAP), unstable angina pectoris (UAP), and acute myocardial infarction (AMI) (Table 1). e levels of hs-CRP (P 0.004), IL-6 (P 0.002), and IL-8 (P 0.002) were significantly increased in the AMI groups compared with the CPS groups. e levels of hs-CRP (P 0.005), IL-6 (P 0.004), and IL-8 (P 0.008) were

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Summary

Introduction

Cardiovascular disease is the leading cause of death throughout the world. e mechanism of coronary artery disease is atherosclerosis (AS), which leads to coronary artery stenosis and myocardial ischemia. MicroRNAs have been demonstrated to be associated with in ammation and cardiovascular disease [4,5,6,7]. E alternation in the expression of microRNAs in some in ammatory diseases has been investigated. Both miR-21 and miR-146a were upregulated in psoriasis [9], whereas miR-146a and miR-155 were upregulated in rheumatoid arthritis [10]. MiR-21, miR-146a, and miR-155 were considered to be in ammation-related microRNAs and are associated with coronary artery disease [11]. Our previous studies has con rmed that the expression of miR155 in peripheral blood mononuclear cells (PBMCs) and plasma was decreased in patients with coronary heart disease, and it was negatively correlated with the severity of the disease and coronary artery lesions assessed by Gensini score [12]. Whether the miR-21, miR-146a, and miR-155 are associated with plaque stability is still unknown

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