,Exosome-encapsulated miR-505 from ox-LDL-treated vascular endothelial cells aggravates atherosclero

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Neutrophil extracellular traps (NETs) play an important role in the pathological process of atherosclerosis (AS).This study aims to evaluate whether exosomes from oxidized low-density lipoprotein (ox-LDL)-treated vascular endothelial cells (VECs) aggravate AS by inducing NET formation.Exosomes from the peripheral blood of healthy donors and AS patients (namely NC-EXO and AS-EXO,respectively) and exosomes from human umbilical vein endothelial cells (HUVECs) treated without or with ox-LDL (namely normal EXO and ox-LDL-EXO,respectively) were isolated,identified,and co-cultured with neutrophils from peripheral blood of healthy donors.NET formation was evaluated by immunofluorescence staining and determining the content of cell-free DNA and myeloperoxidase-DNA complex.Dual-luciferase reporter assay,chromatin immunoprecipitation assay,quantitative reverse transcription polymerase chain reaction,and weste blot analysis were performed to explore the underlying mechanisms.We found that AS-EXO and ox-LDL-EXO induced NET release from neutrophils.Mechanistically,ox-LDL treatment in HUVECs might activate the NF-κB pathway,which transcriptionally activates miR-505,and then the exosome-encapsulated high miR-505 expression targeted and inhibited SIRT3 in neutrophils,thereby inducing reactive oxygen species (ROS) level increase and NET release by neutrophils.Further in vivo experiments showed that ox-LDL-EXO accelerated AS progression in AS mice.In summary,exosome-encapsulated miR-505 from ox-LDL-treated VECs aggravates AS by inducing NET formation.
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