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Objective:To highlight the relationship between miR-503 and wound healing of diabetic foot ulcer (DFU).Methods:Microarray analysis was used to detect the dysregulated miRNAs between the DFU tissues and normal tissues.The expression of miR-503 in tissues and serum of patients with DFU was detected by qRT-PCR technique.Then,CCK-8 assay was applied to determine the cell proliferation.TUNEL assay was used for assessing the apoptosis of cells after treatment with miR-503.Possible correlation between miR-503 and fibillin l (FBN 1) was predicted according to data accessed on RNA22 website online,and was detected for confirmation by luciferase reporter assay.Results:Microarray analysis showed that miR-503 was significantly decreased in the DFU tissues compared with normal tissues.While marked increase in the expression of miR-503 in tissues and serum of patients with DFU was confirmed by qRT-PCR technique.Then,CCK-8 assay indicated that transfection of miR-503 mimic obviously accelerated the cell proliferation.However,TUNEL assays suggested that miR-503 mimic inhibited the apoptosis of cells to improve the survival of fibroblasts.Besides,miR-503 AMO played a role in fibroblasts of DFU tissues exactly countering to miR-503 mimic treatment.It was predicted that MiR-503 is a complementary to the FBN1 by RNA22.Besides,SiRNA-FBN1 promoted the proliferation,but brought down the apoptosis of fibroblasts.Conclusions:MiR-503 regulates the function of fibroblasts and wound healing of patients with DFU by targeting FBN1 directly which provids a novel and critical target for diagnosis and treatment of DFU.