Background: The authors have previously demonstrated that normal mice lacking fibroblast growth factor (FGF)-7 can heal cutaneous wounds normally, likely as a result of various compensatory mechanisms. In this study, the authors explored the role of FGF-7 on wound healing in diabetic mice.
Methods: Full-thickness excisional dorsal wounds were created in FGF-7–null diabetic (FGF-7−/− Leprdb/db, experimental group, n = 8), FGF-7–null (FGF-7−/− Lepr+/+, FGF-7–null group, n = 8), diabetic (FGF-7+/+ Leprdb/db, diabetic group, n = 11), and wild-type (FGF-7+/+ Lepr+/+, wild-type group, n = 11) mice. Wound closure was followed by digital planimetry. Wound tissues were harvested on day 7 for immunohistochemical staining of cell proliferation (Ki67) and real-time polymerase chain reaction.
Results: As expected, the experimental and diabetic groups had significantly slower wound healing than the FGF-7–null or wild-type group. The absence of FGF-7, however, further delayed wound healing in diabetic mice. Curiously, the contraction rate in the experimental group was significantly lower than that in the diabetic group, whereas the epithelialization rate in experimental mice was comparable to that in the diabetic group. Real-time polymerase chain reaction expression of growth factors, including transforming growth factor-β1, basic fibroblast growth factor, and epidermal growth factor in experimental mice, was also generally lower than that in diabetic mice.
Conclusions: Although the lack of FGF-7 did not appear to affect reepithelialization of cutaneous wounds even in diabetic mice, it significantly reduced the wound contraction rate of healing by further altering the dermal components in diabetic mice. Given the specifically targeted effects of FGF-7 on epithelial cells, the authors' findings suggest that further FGF-7–dependent epithelial–mesenchymal interaction exists that may be important in diabetic wound healing.