LAUSR

To investigate the relationship between small noncoding microRNA‐103 (miR‐103) and wound healing of diabetic foot ulcers (DFU) and the underlying molecular mechanism, forty type 2 diabetes mellitus with DFU (DFU group), and 20 patients with a chronic skin ulcer of lower limbs and normal glucose tolerance (SUC group) were included. Quantitative real‐time PCR method was used to determine miR‐103 expression levels in the wound margin tissue of subjects, and to analyse the relationship between the expression of miR‐103 and DFU wound healing. In vitro experiments were also performed to understand the effect of miR‐103 on the high glucose‐induced injury of normal human dermal fibroblasts (NHDFs) cells. The results showed that the miR‐103 expression level in the DFU group was significantly higher than that in the SUC group [5.81 (2.25–9.36) vs 2.08 (1.15–5.72)] (P < 0.05). The expression level of miR‐103 in the wound margin tissue of DFU was negatively correlated with the healing rate of foot ulcers after four weeks (P = 0.037). In vitro experiments revealed that miR‐103 could inhibit the proliferation and migration of NHDF cells and promote the apoptosis of NHDF cells by targeted regulation of regulator of calcineurin 1 (RCAN1) gene expression in a high glucose environment. Down‐regulation of miR‐103 could alleviate high glucose‐induced NHDF cell injury by promoting RCAN1 expression. Therefore, the increased expression of miR‐103 is involved in the functional damage of NHDF cells induced by high‐glucose conditions, which is related to poor wound healing of DFU. These research findings will provide potential targets for the diagnosis and treatment of chronic skin wounds in diabetes.