Resolvin E1 attenuates injury-induced vascular neointimal formation by inhibition of inflammatory responses and vascular smooth muscle cell migration

Mechanical insults, suchas stent implantation, caninduce endothelial injury, vascular inflammation, and ultimately lead to vascular neointimal hyperplasia. Resolvin E1 (RvE1), derived from the v3 fatty acid eicosapentaenoic acid, can facilitate the resolution of inflammation inmany settings. We therefore aimed to determine if therewas a role for RvE1 in preventing neointimal formation after arterial injury and to understand the underlying mechanisms. Vascular inflammation and neointimal hyperplasia were induced by wire injury in the femoral arteries ofmice.Administration of exogenousRvE1 and endogenously generatedRvE1 via dietary supplementation with eicosapentaenoic acid and aspirin markedly reduced vascular neointima formation in this model.Mechanistically, RvE1 was found to inhibit vascular neutrophil infiltration, promotemacrophage polarization toward anM2- like phenotype, suppress T-cell trafficking by reducing RANTES secretion fromvascular smoothmuscle cells, and inhibit vascular smooth muscle cell migration. In summary, RvE1 demonstrated a protective role against vascular inflammation and remodeling in response to mechanical injury, suggesting that it may serve as an adjuvant therapeutic agent for percutaneous coronary interventions, such as stent implantation. © FASEB.