MiR-335-5p expression might induce endothelial cells (ECs) aging and target inhibit . This study aimed to investigate whether oxidative stress evoked miR-335-5p expression and whether miR-335-5p-regulated ECs function through sKlotho. The expression of miR-335-5p was detected in human umbilical vein endothelial cells treated with HO. Subsequently, endothelial function and expression were measured in human umbilical vein endothelial cells treated with HO and transfected with miR-335-5p mimics or inhibitor sequences. Vector containing reporting system of 3'- untranslated region with a miR-335-5p-binding site was constructed. HO stimulation significantly increased miR-335-5p expression. Force overexpression miR-335-5p suppress ECs function and expression. MiR-335-5p target regulated . MiR-335-5p might serve as a negative factor for endothelial homeostasis and a potential treatment target for atherosclerosis.
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