Abstract
Background: The prevalence of coronary heart disease (CHD) appears to be high among Chinese Mongolians. MiR-23b has been proven to play a key role in atherosclerosis. The expression and role of miR-23b in the Mongolians at high cardiovascular risk were explored in the present study.Methods: Forty cases of blood samples from the Mongolians at high cardiovascular risk were enrolled in the present study. The expression of miR-23b was quantified by quantitative real-time PCR. To induce monocytes differentiation into macrophages, HP-1 cells were cultured with phorbol 12-myristate 13-acetate. The level of inflammatory markers was determined by the enzyme-linked immunosorbent assay. The interaction between miR-23b and A20 was explored by the dual luciferase reporter assay.Results: The expression of miR-23b in the Mongolian at high cardiovascular risk was higher than that in healthy Mongolian volunteers. Decrease in ATP-binding cassette transporter A1 caused by miR-23b is responsible for TC accumulation in the Mongolian at high cardiovascular risk. MiR-23b enhanced the oxidized low-density lipoprotein (oxLDL)-induced inflammatory response of THP-1 derived macrophage. MiR-23b regulated nuclear factor-κB (NF-κB) pathway through targeting A20. MiR-23b mediated oxLDL-induced inflammatory response of peripheral blood mononuclear cell in the Mongolian at high cardiovascular risk.Conclusion MiR-23b enhanced oxLDL-induced inflammatory response of macrophages in the Mongolian at high cardiovascular risk through the A20/NF-κB signaling pathway, and thus contributing to atherosclerosis.
Highlights
Coronary heart disease (CHD), called ischemic heart disease, is featured with coronary arteries arteriosclerosis (CAA), which leads to stenosis and obstruction of lumen of the coronary, or coronarospasm, and final acute or temporary myocardial ischemia and anoxia [1]
Liver X receptor α (LXRα) is a nuclear receptor implicated in cholesterol homeostasis, showing pivotal anti-inflammatory roles in atherosclerotic macrophage [23], and LXRα regulates the reverse transport of cholesterol by up-regulating ATP-binding cassette transporter A1 (ABCA1) [24]
In consideration of the high and increasing frequency of coronary heart disease (CHD) and CHD-attributed mortality in the Mongolians, we investigated the expression of miR-23b in serum of the Mongolians at high cardiovascular risk and analyzed the relationship between miR-23b and cardiovascular risk factors
Summary
Coronary heart disease (CHD), called ischemic heart disease, is featured with coronary arteries arteriosclerosis (CAA), which leads to stenosis and obstruction of lumen of the coronary, or coronarospasm, and final acute or temporary myocardial ischemia and anoxia [1]. Macrophage inflammation is the principal element of atherosclerosis c 2018 The Author(s). The expression and role of miR-23b in the Mongolians at high cardiovascular risk were explored in the present study. Methods: Forty cases of blood samples from the Mongolians at high cardiovascular risk were enrolled in the present study. Decrease in ATP-binding cassette transporter A1 caused by miR-23b is responsible for TC accumulation in the Mongolian at high cardiovascular risk. MiR-23b enhanced the oxidized low-density lipoprotein (oxLDL)-induced inflammatory response of THP-1 derived macrophage. MiR-23b mediated oxLDL-induced inflammatory response of peripheral blood mononuclear cell in the Mongolian at high cardiovascular risk. Conclusion MiR-23b enhanced oxLDL-induced inflammatory response of macrophages in the Mongolian at high cardiovascular risk through the A20/NF-κB signaling pathway, and contributing to atherosclerosis
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