Abstract: Objective To study the mechanism of high uric acid (UA) concentration underlying endothelial cell migration via miRNA-663. Methods EA.hy926 cells were incubated in 600 μmol/L uric acid for 48 h. Serum miRNA-663 level in patients with high UA concentration was measured by RT-PCR. The miRNA-663 target gene was identifed by dual luciferase assay. TGF-β₁expression level in endothelial cells was measured. Effect of high UA concentration on endothelial cell migration via miRNA-663 was detected by miR-663 inhibitor and TGF-β₁siRNA transfection and scratch test, respectively. Results The expression level of miRNA-663 was signifcantly higher in endothelial cells after cultured with high UA concentration than before cultured with high UA concentration. The serum miRNA-663 level was signifcantly higher in hyperuricemia patients than in normal subjects. Dual luciferase assay showed that miRNA-663 directly regulated the TGFB1 translation level. Scratch test revealed that high UA concentration signifcantly inhibited the endothelial cell migration and down-regulated the TGF-β₁expression level. The TGF-β₁expression level elevated and the endothelial cell migration increased after the miRNA-663 inhibitors were transfected. However, the miRNA-663 inhibitors could not promote endothelial cell migration when the TGF-β₁expression was inhibited by siRNA. Conclusion High UA concentration inhibits endothelial cell migration by down-regulating TGF-β₁expression via miRNA-663