miR-191-5p inhibits angiogenesis in diabetic foot ulcers wound healing via regulating VEGFA

Diabetic foot ulcer (DFU) is a severe complication of diabetes mellitus (DM). The present study aimed to explore the role of miR-191-5p and its target VEGFA in the DFU.

207 Volunteers were recruited including 105 uncomplicated DM patients and 102 DFU patients. The expression of miR-191-5p and VEGFA were quantified by qRT-PCR. VEGFA protein level was assayed by Western blot. Pearson correlation, ROC curve, and logistic regression evaluated the clinical relevance, diagnostic potential, and risk factors, respectively. High-glucose stimulated Human umbilical vein endothelial cells (HUVEC). Proliferation and migration capability were assayed by CCK-8 and Transwell in HUVEC. The target relationship was assessed by dual-luciferase reporter assay.

miR-191-5p was enhanced in serum and HG-induced HUVEC and identified as an independent risk factor. miR-191-5p abundance was positively associated with the DFU area, CRP, WBC, and NEUT. Downregulation of miR-191-5p inhibited the HUVEC migration and proliferation potential and mRNA expression of PDGF-, PDGFR-β, and FGF-2. VEGFA was predicted and verified as a target of miR-191-5p. VEGFA abundance was negatively related to miR-191-5p. miR-191-5p impeded HUVEC migration, proliferation, and angiogenesis by regulating VEGFA.

In summary, miR-191-5p was related to DFU progression and promoted DFR development. As a potential biomarker, miR-191-5p impeded HUVEC migration, proliferation, and angiogenesis by regulating the target VEGFA.