Background:Vein graft failure (VGF) is a serious complication of coronary artery bypass graft,although the mechanism remains unclear.The study aimed to investigate the effects of microRNAs (miRNAs) on the endothelial dysfunction involved in VGF.Methods:Human umbilical vein endothelial cells (HUVECs) were subjected to mechanical stretch stimulation to induce endothelial dysfunction.Genome-wide transcriptome profiling was performed using the Human miRNA OneArray~ V4 (PhalanxBio Inc.,San Diego,USA).The miRNA-messenger RNA (mRNA) network was investigated using gene ontology and Kyoto Encyclopedia of Genes and Genomes.The miR-551 b-5p mimic and inhibitor were applied to regulate miR-551 b-5p expression in the HUVECs.The 5-ethyuyl-2'-deoxyuridine assay,polymerase chain reaction (PCR),and Western blotting (WB) were used to assess HUVECs proliferation,mRNA expression,and protein expression,respectively.The vein graft model was established in early growth response (Egr)-l knockout (KO) mice and wide-type (WT) C57BL/6J mice for pathological and immunohistochemical analysis.Endothelial cells isolated from the veins of WT and Egr-1 KO mice were subjected to mechanical stretch stimulation;PCR and WB were conducted to confirm the regulatory effect of Egr-1 on Intercellular adhesion molecule (Icam-1).One-way analysis of variance and independent t-test were performed for data analysis.Results:Thirty-eight miRNAs were differentially expressed in HUVECs after mechanical stretch stimulation.The bioinformatics analysis revealed that Egr-1 might be involved in VGF and wvas a potential target gene of miR-55 lb-5p.The mechanical stretch stimulation increased miR-55 lb-5p expression by 2.93 ± 0.08 fold (t =3.07,P ＜ 0.05),compared with the normal HUVECs.Transfection with the miR-551b-5p mimic or inhibitor increased expression of miR-551b-5p by 793.1 ± 171.6 fold (t =13.84,P ＜ 0.001) or decreased by 26.3％ ± 2.4％ (t 26.39,P ＜ 0.05) in the HUVECs,respectively.HUVECs proliferation and EGR-1 mRNA expression were significantly suppressed by inhibiting miR-55 lb-5p expression (P ＜ 0.05).The lumens of the vein grafts in the Egr-1 KO mice were wider than that in the WT mice.Icam-1 expression was suppressed significantly in the Egr-1 KO vein grafts (P ＜ 0.05).Conclusions:Increased miR-551b-5p expression leads to endothelial dysfunction by upregulating Egr-1 expression.EGR-1 KO can improve the function of a grafted vein through suppressing Icam-1.