Localization of MMP and TIMP on the chronic skin wounds and possible application of MMP inhibitor

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The functions and regulations of MMPs and MMPs on the wound healing process are not fully understood. The lack of experimental models for chronic wounds is the main problem for the evaluation. We evaluated the functions of MMPs using pressure ulcer tissues. At the edge of epithelization, MMP2 and MMP9 are upregulated in the epithelial cells between basal layer to granular layers. In the middle area of pressure ulcer, MMPs and TIMPs are not found. Along with epithelization, wound fibroblast and wound macrophage expressed MMP2 and MMP9 and TIMP2. For the development of animal model, we evaluated wound healing in the chronic renal failure rat and cinnamon mouse. Delay of wound healing of incisional wound and full thickness wound was not observed in the chronic renal failure rat. Delay in the wound healing was observed in cinnamon mouse. The final study was to observe whether biofilm formation occurs on skin wounds. Full or partial thickness wounds were created on the backs of SD rats. Suspensions of P.aeruginosa (PAO1 carrying the gene encoding the green fluorescent protein) was applied on the wounded area. Wounds were harvested and processed for histology and immunohistochemistry. The presence of biofilm were indicated Rhodamine-conjugated concanavalin A. We confirmed biofilm formation by P.aeruginosa on skin wounds can observe in this experimental model, and partial thickness wounds were proper for to observe biofilm formation. Also, a standardized dorsal ischemic flap was lifted and sutured. Partial thickness wounds were created on the flap. The extent of biofilm formation was significantly diminished on the surface of ischemic wound compared with non-ischemic control. Wound ischemia in the experimental model does not increase the formation of biofilms.