Document Type

Article

Publication Date

Fall 10-5-2026

Abstract

Background: Atherosclerosis is a chronic inflammatory disease in which monocyte-endothelial interactions contribute to early plaque development through inflammatory activation of endothelial adhesion molecules, including ICAM-1 and VCAM-1. Although the GLP-1 receptor agonist semaglutide reduces cardiovascular events clinically, its direct effects on inflammatory monocyte-endothelial interactions remain unclear. Objective: To establish an in vitro model of monocyte-endothelial interactions under inflammatory conditions and investigate whether semaglutide reduces TNF-α-induced monocyte adhesion and migration across activated endothelial cells. Methods: EA.hy926 endothelial cells and THP-1 monocytes were cultured under optimized conditions. TNF-αwas used to induce endothelial inflammation, with PBS as a negative control and atorvastatin as a positive control. Monocyte adhesion was initially evaluated by microscopy in a pilot assay. Calcein AM fluorescence labeling was subsequently incorporated to enable accurate visualization and quantification of adherent monocytes. Ongoing studies use Transwell migration assays and fluorescence microscopy to evaluate the effects of semaglutide on monocyte adhesion, transmigration, and endothelial ICAM-1/VCAM-1 expression. Results: Cell culture conditions for EA.hy926 endothelial cells and THP-1 monocytes were successfully established, and treatment conditions for TNF-αand semaglutide were optimized through preliminary experiments. The pilot adhesion assay confirmed that THP-1 monocytes attach to the endothelial monolayer. Fluorescent labeling was incorporated into subsequent experiments to improve discrimination and quantitative assessment of monocyte adhesion. Conclusions: An in vitro monocyte-endothelial interaction model has been successfully established and optimized for evaluating inflammatory cell adhesion and

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