Abstract

BackgroundKnowledge of stenosis in coronary arteries requires an understanding of the cellular and molecular processes that occur throughout the leukocyte rolling process. In this study, the roles of miR-125a-5p and miR-495-3p were investigated on the adhesion of endothelial cells (ECs) isolated from the human aorta.MethodsHuman primary endothelial cells were obtained from the aorta of people who had died of brain death. Whole blood was used to isolate the monocytes. The miR-125 and miR-495 were predicted and transfected into ECs using Poly Ethylene Imine (PEI). The expression levels of adhesion molecules and monocyte recruitment were identified by the RT-qPCR technique and Leukocyte-Endothelial Adhesion Assay kit, respectively.ResultsThe ICAM-1, ICAM-2 and VCAM-1 expression levels decreased significantly in the miR-495/PEI-transfected ECs (P < 0.05) while in the miR-125/PEI-transfected ECs only the ICAM-2 and ITGB-2 expression levels decreased significantly (P < 0.05) as compared to the miR-synthetic/PEI-transfected ECs. Furthermore, the monocyte adhesion was decreased in the miR-125 and miR-mix/PEI-transfected ECs as compared to the miR-synthetic/PEI-transfected ECs (P = 0.01 and P = 0.04, respectively).ConclusionAccording to the findings, the efficient relations between miR-125 and adhesion molecules may be responsible for the inhibition of monocyte rolling.

Highlights

  • Atherosclerosis is the leading cause of death from cardiovascular diseases (CVD) worldwide [1, 2]

  • MiR‐125 and miR‐495 decrease ICAM‐2 gene expression The results showed that the ICAM-2 gene expression levels decrease significantly in miR-125 and miR-495/ Poly Ethylene Imine (PEI)-transfected endothelial cells (ECs) as compared to miR-synthetic/

  • MiR‐125 decreases ITGB‐2 gene expression The ITGB-2 gene expression level decreased in miR-125/ PEI-transfected ECs as compared to miR-synthetic/PEItransfected ECs (p 0.001)

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Summary

Introduction

Atherosclerosis is the leading cause of death from cardiovascular diseases (CVD) worldwide [1, 2]. In addition to the influence of lifestyle, several artery cellular dysfunctions are linked to the development of atherosclerosis [3]. The sub-endothelial macrophages, vascular smooth muscle cells (VSMCs), and endothelial cells (ECs) are the most important agents involved in the initiation and progression of atherosclerotic plaques in the heart arteries [4, 5]. It is well known that miRNAs regulate the function of vascular smooth muscle cells (VSMCs) and modulate the inflammatory responses in vascular endothelial cells so that these events affect vessel stenosis and restenosis [10,11,12,13]. The miRNAs are said to have many roles in the functional balance of vascular endothelial cells and circulating leucocytes via biological pathways and inflammatory responses [24]. The roles of miR-125a-5p and miR-495-3p were investigated on the adhesion of endothelial cells (ECs) isolated from the human aorta

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