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A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes
Published on: February 17, 2023
MicroRNA-21-3p accelerates diabetic wound healing in mice by downregulating SPRY1
Yaohong Wu1, Kun Zhang2, Rong Liu3
1Department of Orthopedics, The Affiliated Ganzhou Hospital of Nanchang University, Ganzhou 341000, Jiangxi, China.
Abstract:
A variety of novel drugs and advanced therapeutic strategies have been developed for diabetic foot ulcers (DFUs); however, the clinical outcomes are unsatisfactory and the underlying mechanisms of DFU remain elusive. MicroRNAs (miRNA) regulate the pathological processes of many diseases. Fibroblasts are involved in each stage of wound healing, and the functions of fibroblasts may be regulated by miRNAs. In the present study, we found that the levels of miRNA-21-3p (miR-21-3p) were decreased in patients with diabetes as compared with those in the healthy control. Similarly, the level of miRNA-21-3p was decreased in fibroblasts that were stimulated with D-glucose as compared with that in the control fibroblasts. Furthermore, enhanced function was found in fibroblasts followed by the miR-21-3p agonist treatment, and a rapid wound healing process was achieved in the miR-21-3p agonist-treated mice. MiR-21-3p directly targeted protein sprout homolog 1 (SPRY1), and the miR-21-3p-regulated reduction in SPRY1 enhanced the function of fibroblasts and accelerated wound healing in vivo. These findings suggest that miR-21-3p may treat DFU by reducing SPRY1.
Insights
MicroRNA-21-3p (miR-21-3p) levels are reduced in diabetic foot ulcers (DFU). Restoring miR-21-3p enhances fibroblast function and accelerates wound healing by targeting SPRY1, suggesting a novel therapeutic approach for DFU.
Area of Science:
- Biomedical Science
- Molecular Biology
- Regenerative Medicine
Background:
- Diabetic foot ulcers (DFU) present a significant clinical challenge with unsatisfactory outcomes.
- The underlying mechanisms of DFU pathogenesis remain incompletely understood.
- MicroRNAs (miRNAs) are key regulators in disease processes, including wound healing.
Purpose of the Study:
- To investigate the role of microRNA-21-3p (miR-21-3p) in diabetic foot ulcer development.
- To explore the potential of miR-21-3p as a therapeutic agent for DFU.
Main Methods:
- Quantification of miR-21-3p levels in diabetic patients and glucose-stimulated fibroblasts.
- Assessment of fibroblast function following miR-21-3p modulation.
- In vivo wound healing studies in mice treated with miR-21-3p agonists.
- Identification of miR-21-3p target genes.
Main Results:
- miR-21-3p levels were significantly decreased in DFU patients and glucose-treated fibroblasts.
- miR-21-3p agonist treatment enhanced fibroblast function and accelerated wound healing in vivo.
- miR-21-3p was found to directly target and downregulate protein sprout homolog 1 (SPRY1).
- Reduced SPRY1 expression by miR-21-3p promoted fibroblast function and wound repair.
Conclusions:
- Decreased miR-21-3p is implicated in the pathophysiology of diabetic foot ulcers.
- Restoring miR-21-3p levels, potentially by targeting SPRY1, offers a promising therapeutic strategy for DFU treatment.
