Aim
High circulating free fatty acid (FFA) concentration has a critical role in the development of obesity associated vascular comorbidities. Ample previous findings revealed that FFA, especially saturated, induce endothelial dysfunction throught multiple mechanisms (summarized as lipotoxicity). As a mediator that transfers information among cells, extracellular vesicles(EVs) participate in pathologic processes of many diseases, including angiocardiopathy, insulin resistance, autoimmunity disease. However, how lipotoxicity changed the proportion of EVs secreted from monocytes, furthermore, the effect of the EVs exerts on endothelial cells, haven't been demonstrated. Method: In our experience, differential ultracentrifugation was used to extract EVs from condition medium (CM) of THP-1 monocytes under given treatments. Then we co-incubated the EVs derived from palmitate-treated monocytes with HUVECs for 24 h, after which molecular and phenotypic assays were conducted. Result: Palmitate-treated monocytes EVs promote the production of adhesion associated proteins of endothelial cells, such as VCAM-1, ICAM-1. Meanwhile, palmitate-stimulation may play a promoter role in the pro-migration capacity of monocytes-EVs. In brief, EVs could be the new pathological junction between FFA and endothelial damage.