“
TL;DR
This preclinical study used human endothelial cells and diabetic mice to investigate how macrophage-derived small extracellular vesicles containing miR-503 impair endothelial function and wound healing by targeting IGF1R.
Frontiers in Immunology · 6 authors, 2 centres
This summary was generated by AI from a single paper. It has not been reviewed by a clinician and is not clinical advice. Verify against the source before acting on it.
This preclinical study used human endothelial cells and diabetic mice to investigate how macrophage-derived small extracellular vesicles containing miR-503 impair endothelial function and wound healing by targeting IGF1R.
The study investigated the role of M1 macrophage-derived small extracellular vesicles (sEVs) in endothelial dysfunction and impaired wound healing in a diabetic context. In vitro, high-glucose stimulation promoted M1 polarization in macrophages and increased secretion of sEVs containing miR-503, which were taken up by HUVECs. These sEVs impaired HUVEC viability, tube formation, and migration by targeting and inhibiting IGF1R expression. The RNA-binding protein ACO1 was found to mediate miR-503 packaging into sEVs. In vivo, using a skin wound model in diabetic mice, administration of sEVs from miR-503-inhibited macrophages improved wound healing, while IGF1R knockdown hindered it. The study is preclinical, using human cell lines and an animal model, and suggests a mechanistic pathway (miR-503/IGF1R) through which M1 macrophages may impair angiogenesis and healing in diabetic foot ulcers.