Endothelial exosomes work as a functional mediator to activate macrophages

Introduction Intercellular communication is essential for almost all physiological and pathological processes. Endothelial cell (EC)-derived exosomes, working as mediators intercellular information exchange, are involved in the pathophysiological mechanisms of atherosclerosis. However, effect inflamed endothelial exosomes on function macrophages (Mϕ) poorly defined. This study aims to unravel how derived from tumor necrosis factor-α (TNF-α)-stimulated ECs (exo-T) affect Mϕ vitro . Methods results Exosomes untreated (exo) exo-T were identified by using TEM, NTA, western blot, we observed that PKH67-labeled exo/exo-T taken up Mϕ. Exposure 24 h not only skewed M1 subtype exacerbated lipid deposition, but also promoted apoptosis, while it did significantly migration, detected RT-qPCR, Dil-ox-LDL uptake assay, flow cytometry, wound healing transwell respectively. In addition, exo/exo-T-related microRNA-Seq revealed 104 differentially expressed microRNAs (DE-miRNAs). The target genes DE-miRNAs mainly enriched functionally metabolic pathways, MAPK signaling pathway, etc., determined Gene Ontology (GO) Kyoto Encyclopedia Genes Genomes (KEGG) pathway analyses. We further demonstrated immunoblotting intervention improves phosphorylation MAPK/NF-κB-related proteins. Discussion conclusion Collectively, this reveals (TNF-α-stimulated EC-derived exosomes) work a functional mediator may activate through MAPK/NF-κB pathways.