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Loss of CXC chemokine receptor 3 signaling cause a delay in epidermal and dermal maturation and leads to hypertrophic scarring

CXCR3 and its ligands modulate the timing of keratinocytes migration, fibroblasts and endothelial cell immigration into the wound and epidermal and matrix maturation during wound healing. To investigated the long term effects of CXCR3 in wound healing full thickness excisional wounds were created on CXCR3−/− or wildtype mice and examined at 180 days. Grossly the CXCR3−/− mice presented a thick keratinized eschar compared to the wildtype mice that had a scarcely noticeable scar. Histological analysis of the CXCR3−/− mice also revealed a thicker epidermis that was hyperproliferative, dermal layers that were disorganized with thick and long collagen fibrils, and contained excessive collagen content in comparison to the wildtype mice. Interestingly, the CXCR3−/− wounds results in a weaker tensile strength as a result of decreased cross‐linking of collagen fibers. A lack of ECM turnover was shown by the elevated expression of matrix proteins tenascin C, fibronectin, and an imbalance of MMP‐9 expression; these were noted as late as 180 days postwounding, whereas these markers of an immature dermis are long gone in wounds in wildtype mice. These in vivo studies establish that the absence of the CXCR3 signaling network results in hypertrophic scarring by delaying maturation and altering the synthesis and degradation of collagen in addition to other matrix components during wound healing. Supported by grants from the NIH