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MICROMouse Program Application Abstract

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Development of a mouse model of diabetic wound healing

Efi Kokkotou (Boston, MA)

MICROMouse Program

Diabetic foot ulcers remain a costly and disabling clinical problem with no established treatment, mainly due to the lack of suitable animal models the study of which will shed light into the underlying mechanisms of impaired wound healing in diabetes, and in parallel will allow the development and testing of new therapies. It is accepted that peripheral neuropathy and microvascular disease are major diabetic complications that prevent complete wound closure. Substance P (SP) is an 11-aminoacid neuropeptide that has been implicated in pain perception and neurogenic inflammation, mainly acting via its receptor NK-1R. We thus hypothesized that NK-1R deficient mice with sensory neuropathy might represent a model of impaired wound healing that closely approximates the human condition. Our preliminary studies clearly demonstrate that wound closure is delayed in these mice, even in the absence of diabetes. We have also discovered that at baseline, the NK-1R knockout mice have reduced skin oxygenation, another shared feature with diabetic patients. We propose to perform a comprehensive analysis of wound healing in the NK-1R deficient mice and compare their phenotype with other frequently used diabetic mouse models which will be treated with SP or a SP- antagonist. Upon its complete characterization, the simplicity and reproducibility of our proposed model of diabetic wound healing will provide researchers in the field with a valuable tool to further study mechanisms of wound healing and how these are compromised in uncontrolled diabetes. It will also provide a platform for efficient evaluation of novel treatments for diabetic ulcers, and skin wounds in general.

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