Zhao and coworkers continue strengthening the research toward companion diagnostics with these strong data supporting assessing micro-RNA 103 (miRNA 103) levels in tissue margins.
Changes in miroRNA103 expression in wound margin tissue are related to wound healing of diabetes foot ulcers
- microRNAs (miRNAs) are involved in the regulation of wound healing
- to investigate the relationship between miR-103, wound healing of diabetic foot ulcers (DFU), and the underlying molecular mechanism, forty type 2 diabetes mellitus with DFU (DFU group), 20 patients with chronic skin ulcer of lower limbs, and normal glucose tolerance (SUC group) were included
- in vitro experiments were performed to understand the effect of miR-103 on the high glucose-induced injury of human dermal fibroblasts cells
- the increased expression of miR-103 in wound margin tissue of DFU may be associated with poor wound healing
- the miR-103 is involved in the high glucose-induced functional impairment in dermal fibroblasts through targeted regulation of regulator of calcineurin 1 (RCAN1) expression
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.
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