Adhesion of monocytes and endothelial cells isolated from the human aorta suppresses by miRNA-PEI particles

Abstract

Background Knowledge 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. Methods Human 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. Results The 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). Conclusion According to the findings, the efficient relations between miR-125 and adhesion molecules may be responsible for the inhibition of monocyte rolling.

miR-27a inhibits molecular adhesion between monocytes and human umbilical vein endothelial cells; systemic approach

“…The activated endothelial cells might overexpress adhesion molecules and enhance leukocyte adhesion following rolling, strong adhesion, crawling, and transmigration processes [7]. Many studies showed that non-coding RNAs target the adhesion molecules and other genes involved in vessel stenosis [20][21][22][23][24]. This study was focused on the effects of miRNA-related genes predicted Fig.…”

“…Finally, macrophages by production of matrix metalloproteinase enzymes (MMPs) degrade the extracellular matrix (ECM), causing plaque remodeling [1-3, 5, 6]. In the other hand, micro-RNAs (miRNA/miR) are small nucleotides that affect the cellular pathways via the regulation of gene expression levels [13,20,21]. Many studies reported that micro-RNAs might retard atherosclerosis process by targeting some genes such as adhesion molecules [20,22].…”

“…In the other hand, micro-RNAs (miRNA/miR) are small nucleotides that affect the cellular pathways via the regulation of gene expression levels [13,20,21]. Many studies reported that micro-RNAs might retard atherosclerosis process by targeting some genes such as adhesion molecules [20,22]. In this study, miR-194 and miR-27a were predicted using miRNA-gene databases and monocyte-endothelial adhesion was evaluated through the changes of P-selectin, E-selectin, and JAM-B gene expression levels.…”

Cellular crosstalk in atherosclerotic plaque microenvironment

“…As indicated in the above, the neutrophils, leukocytes, and T cells migrate through activated arterial walls, which is a prerequisite step due to the infection or damage [ 32 ]. The entry of cells into the inflamed locations occurs in several stages including the weak adhesion, rolling, and crawling between endothelial cells and leukocytes [ 8 , 33 ] (Fig. 1 ).…”

PbO Nanoparticles Increase the Expression of ICAM-1 and VCAM-1 by Increasing Reactive Oxygen Species Production in Rat Choroidal Epithelial Line Z310 Cells

“…VCAM-1 can regulate the in ammatory response of endothelial cells in the whole body and promote the migration of leukocytes after binding to integrin receptor α4β1 (Yousef et al, 2019).Under physiological condition, the expression levels of ICAM-1 and VCAM-1 are relatively low. Environmental stimuli upregulate the expression of these adhesion molecules (Poursaleh et al, 2021;Shen et al, 2021). ICAM-1 and VCAM-1 also participate in BBB permeability change (Walter et al, 2022).…”