pkh-26 and Wounds-and-Injuries

Non-healing diabetic wounds are difficult to treat. They also create heavy financial burdens for both patients and society. Negative pressure wound therapy (NPWT) has been adopted to treat intractable wounds and has proved to be effective. However, the mechanisms that underlie the effects of this treatment are not entirely understood. Circulating fibrocytes are unique haematopoietic-derived stem cells that have been reported to play a pivotal role in wound healing. Here, we have investigated the effect of NPWT on fibrocyte mobilization and the role of fibrocyte mobilization in the healing of diabetic wounds during NPWT. We show that the NPWT group exhibited 2.6-fold to 12.1-fold greater numbers of tail vein-injected PKH-26-labelled fibrocytes in the diabetic wound sites compared with the control group. We also demonstrate that the full-thickness skin wounds treated with NPWT exhibit significantly reduced mRNA and protein expression, blood vessel density and proliferating cells when exogenous fibrocyte mobilization is inhibited. We speculate that systemic mobilization of fibrocytes during NPWT may be a mechanism for healing intractable wounds in a diabetic rat model experiment and that enhancement of cell mobilization may represent a potential treatment idea for intractable wound healing across all fields of surgery.

Topics: Animals; Chemokine CXCL12; Collagen Type I; Diabetes Mellitus, Experimental; Fluorescent Dyes; Gene Expression Regulation; Male; Mesenchymal Stem Cells; Negative-Pressure Wound Therapy; Organic Chemicals; Platelet-Derived Growth Factor; Rats; Rats, Sprague-Dawley; Signal Transduction; Staining and Labeling; Streptozocin; Transforming Growth Factor beta1; Vascular Endothelial Growth Factor A; Wound Healing; Wounds and Injuries