miR-10b-5p targets TGFBR1 to promote keratinocyte-mediated wound healing in diabetic patients and has predictive prognostic value.

BACKGROUND

Diabetic wounds are known for their poor healing outcomes, and microRNAs (miRNAs) have emerged as key regulators of the wound healing process.

AIM: To investigate miR-10b-5p's predictive value in diabetic wound healing and the potential molecular mechanisms underlying its influence on the healing process.

MATERIALS AND

METHODS

Samples from patients with diabetic wounds were collected and divided into two groups: the good healing group and the delayed healing group. RT-qPCR was used to detect the levels of miR-10b-5p, TGFBR1 and VEGF. A ROC curve was used to evaluate the ability of miR-10b-5p to predict delayed wound healing in diabetic patients. Stimulation of HaCaT cells with 30 mM d-glucose mimics the pathological characteristics of diabetic skin wounds. The proliferation, apoptosis and migration of HaCaT cells were evaluated by CCK-8, flow cytometry and scratch assay. The database prediction, Pearson analysis, and dual luciferase assay demonstrated the targeting relationship between miR-10b-5p and TGFBR1.

RESULTS

In the delayed healing tissues, miR-10b-5p is downregulated while TGFBR1 is upregulated. miR-10b-5p can accurately predict the wound healing outcome of diabetes patients (AUC = 0.910, Sensitivity = 84.70 %, Specificity = 79.30 %). An HG environment inhibited the proliferation and migration of HaCaT cells and induced apoptosis. Overexpression of TGFBR1 reversed the effects of miR-10b-5p overexpression on the proliferation, apoptosis, migration and VEGF expression of HaCaT cells.

CONCLUSION

miR-10b-5p has good predictive value for diabetic wound healing and regulates HaCaT cell-mediated re-epithelialization by targeting TGFBR1.