The Tie-2 agonist PMC-403 inhibits endothelial damage induced by e-cigarette vapor or LPS

Background

The use of e-cigarettes is currently increasing despite potential harmful effects of e-cigarettes. Acute e-cigarette exposure may cause endothelial damage thereby contributing to acute lung injury or vascular dysfunction after chronic use. These effects may be enhanced by concomitant inflammatory stimuli. We investigated the acute effect of e-cigarette vapor (ECV) with or without concomitant lipopolysaccharide (LPS) stimulation on endothelial cell function in vitro and on vascular permeability in isolated lungs. Further potentially protective effects of the Tie2 agonist PMC-403 were studied.