Currently, most available healthcare options address wound management, but not therapy of these diabetic wounds. This monetary value, however, does not account for psychosocial and economic impacts on the quality of life for both patients and caregivers. Chronic non-healing ulcers are one of the most conspicuous manifestations of this disease, costing an estimated $1.38 billion annually. Diabetes and associated complications affect 9.4% of the population of the United States, or 1 in every 11 individuals. The urgent need for effective treatment of chronic diabetic ulcers has seen a surge in utilization of mesenchymal cells with primitive stem-like properties. In addition, investigations concerning safety and efficacy of this therapy in clinical trials should be pursued. Future studies should be aimed towards validating our observations through further examination of the paracrine potential of AFMSCs. Since vehicle-treated diabetic wounds did not demonstrate accelerated healing, we determined that AFMSCs were therapeutic through their paracrine activities. Treatment of diabetic wounds using amniotic fluid-derived MSCs encourages cutaneous tissue repair through affecting inflammatory cell behavior in the wound site. We found no evidence of AFMSC engraftment or biotherapy induced immune response. In addition, AFMSC treatment induced changes in the profiles of macrophage polarizing cytokines, resulting in a change in macrophage composition in the diabetic wound bed. This was significantly lower than the vehicle-treated diabetic wounds, which required on average 27.5 days to heal (p < 0.01), and most similar to time of closure in wild type untreated wounds (an average of around 18 days). ResultĪverage time to wound closure was approximately 19 days in AFMSC-treated diabetic wounds. A priori statistical analyses measures determined significance of the data. Post-treatment, we compared healing time and molecular and cellular events of AFMSC-treated, vehicle-treated, untreated diabetic, and non-diabetic wounds. Immediately after wounding, we applied AFMSCs topically to the sites of injuries on diabetic mice, while media application only, defined as vehicle, served as controls. We then generated 10 mm wounds in Lepr db/db diabetic mouse skin, and splinted them open to allow for humanized wound modeling. We obtained third trimester amniotic fluid from term cesarean delivery and isolated and expanded MSCs in vitro. Here, we investigate the potential of amniotic fluid-derived multipotent stromal cells (AFMSCs) to restore molecular integrity to diabetic wounds, amend pathology and promote wound healing. Amniotic fluid presents a relatively unexplored source of MSCs and one with wide availability. However, variations in sources and access are limiting factors for broader adaptation and study of MSC-based therapies. Multipotent stromal cells (MSCs) have been touted as a powerful new therapy for diabetic tissue repair owing to their trophic activity and low immunogenicity.
Cutaneous wounds in patients with diabetes exhibit impaired healing due to physiological impediments and conventional care options are severely limited.
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