Abstract
Diabetes can impair wound closure, which can give rise to major clinical problems. Most treatments for wound repair in diabetes remain ineffective. This study aimed to investigate the influence on wound closure of treatments using expanded human cord blood CD34+ cells (CB-CD34+ cells), freshly isolated CB-CD34+ cells and a cytokine cocktail. The test subjects were mice with streptozotocin-induced diabetes. Wounds treated with fresh CB-CD34+ cells showed more rapid repair than mice given the PBS control. Injection of expanded CB-CD34+ cells improved wound closure significantly, whereas the injection of the cytokine cocktail alone did not improve wound repair. The results also demonstrated a significant decrease in epithelial gaps and advanced re-epithelialization over the wound bed area after treatment with either expanded CB-CD34+ cells or freshly isolated cells compared with the control. In addition, treatments with both CB-CD34+ cells and the cytokine cocktail were shown to promote recruitment of CD31+-endothelial cells in the wounds. Both the CB-CD34+ cell population and the cytokine treatments also enhanced the recruitment of CD68-positive cells in the early stages (day 3) of treatment compared with PBS control, although the degree of this enhancement was found to decline in the later stages (day 9). These results demonstrated that expanded CB-CD34+ cells or freshly isolated CB-CD34+ cells could accelerate wound repair by increasing the recruitment of macrophages and capillaries and the reepithelialization over the wound bed area. Our data suggest an effective role in wound closure for both ex vivo expanded CB-CD34+ cells and freshly isolated cells, and these may serve as therapeutic options for wound treatment for diabetic patients. Wound closure acceleration by expanded CB-CD34+ cells also breaks the insufficient quantity obstacle of stem cells per unit of cord blood and other stem cell sources, which indicates a broader potential for autologous transplantation.Electronic Supplementary MaterialSupplementary material is available for this article at 10.2478/s11658-013-0089-9 and is accessible for authorized users.
Highlights
Diabetes is a chronic progressive disease with rising incidence worldwide over the last three decades [1, 2]
Delayed wound closure in diabetes is mainly caused by immune system defects that result in chronic wound problems
We investigated the wound closure capacity of expanded cord blood (CB)-CD34+ cells and freshly isolated CB-CD34+ cells in diabetic mice
Summary
Diabetes is a chronic progressive disease with rising incidence worldwide over the last three decades [1, 2]. One of the major complications of diabetes mellitus is abnormal wound closure and healing, in the case of foot ulcers. This can result in clinical problems, including lower-limb amputation, prolonged hospitalization and lifethreatening sepsis [1]. Factors thought to play key roles in the delay of wound closure and healing in diabetes mellitus include: cellular dysfunction; alterations in growth factor; alterations in the signals that impair the migration and proliferation of keratinocytes and fibroblasts, the production of extracellular matrix, and angiogenesis; and the susceptibility of wound tissue to bacteria and infection [6, 13, 14]. Neuropeptides influence the stimulation of cell chemotaxis, proliferation and growth factor production [1]
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