ArticleRespiratory research2026
The Tie-2 agonist PMC-403 inhibits endothelial damage induced by e-cigarette vapor or LPS.
Article in Respiratory research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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12 authors.
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Abstract
backgroundThe 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.
methodsHuman umbilical cord endothelial cells (HUVECs) were cultured with different types of ECV extracts (ECVE) and/or LPS, and endothelial activation was determined in vitro by measuring secreted protein and mRNA levels of angiopoietin-2 (Angpt-2) and soluble Tie2 (sTie2). Barrier dysfunction was analyzed by continuous transendothelial electrical resistance (TER) measurements using electric cell-substrate impendence sensing (ECIS). An ex vivo isolated mouse lung model was used to analyze endothelial permeability and edema formation upon intratracheal ECV exposure. The Tie2 agonist PMC-403 was applied in vitro and ex vivo and its effect on endothelial permeability was determined.
resultsAngpt-2 secretion and transcription were significantly increased in HUVECs after 24h stimulation with nicotine-containing ECVE (ECVE
conclusionsECV
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