Nuclear factor kappa B (NF-κB) activation contributes to many vascular inflammatory diseases.The present study tested the hypothesis that microRNA-17-3p (miR-17-3p) suppresses the pro-inflammatory responses via NF-κB signaling in vascular endothelium.Human umbilical vein endothelial cells (HUVECs),transfected with or without miR-17-3p agomir/antagomir,were exposed to lipopolysaccharide (LPS),and the inflammatory responses were determined.The cellular target of miR-17-3p was examined with dual-luciferase reporter assay.Mice were treated with miR-17-3p agomir and the degree of LPS-induced inflammation was determined.In HUVECs,LPS caused upregulation of miR-17-3p.Overexpression of miR-17-3p in HUVECs inhibited NIK and IKKβ binding protein (NIBP) protein expression and suppressed LPS-induced phosphorylation of inhibitor of kappa Bα(IKBα) and NF-κB-p65.The reduced NF-κB activity was paralleled by decreased protein levels of NF-κB-target gene products including pro-inflammatory cytokine[interleukin 6],chemokines[interleukin 8 and monocyte chemoattractant protein-1]and adhesiorn molecules[vascular cell adhesion molecule-1,intercellular adhesion molecule-1 and E-selectin].Immunostaining revealed that overexpression of miR-17-3p reduced monocyte adhesion to LPS-stimulated endothelial cells.Inhibition of miR-17-3p with antagomir has the opposite effect on LPS-induced inflammatory responses in HUVECs.The anti-inflammatory effect of miR-17-3p was mimicked by NIBP knockdown.In mice treated with LPS,miR-17-3p expression was significantly increased.Systemic administration of miR-17-3p for 3 days suppressed LPS-induced NF-κB activation and monocyte adhesion to endothelium in lung tissues of the mice.In conclusion,miR-17-3p inhibits LPS-induced NF-κB activation in HUVECs by targeting NIBP.The findings therefore suggest that miR-17-3p is a potential therapeutic target/agent in the management of vascular inflammatory diseases.