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Updated: May 27, 2026
A Protocol for Constructing a Rat Wound Model of Type 1 Diabetes
Published on: February 17, 2023
Lack of FGF-7 further delays cutaneous wound healing in diabetic mice
Cheng Peng1, Bin Chen, Huang-Kai Kao
1Boston, Mass.; Changsha, Hunan, and Kunming, Yunnan, People's Republic of China; and Taoyuan, Taiwan From the Division of Plastic Surgery and the Department of Pathology, Brigham and Women's Hospital, Harvard Medical School; the Department of Burns and Plastic Surgery, the Third Xiangya Hospital of Central South University; the Burns Research Center of Yunnan Province, The Second Affiliated Hospital of Kunming Medical College; and the Department of Plastic Surgery, Chang Gung Memorial Hospital.
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 Lepr, experimental group, n = 8), FGF-7-null (FGF-7 Lepr, FGF-7-null group, n = 8), diabetic (FGF-7 Lepr, 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.
Insights
Fibroblast growth factor-7 (FGF-7) absence delays diabetic wound healing, particularly contraction, suggesting FGF-7 is crucial for dermal repair in diabetes. This highlights FGF-7-dependent epithelial-mesenchymal interactions in diabetic wound healing.
Area of Science:
- Regenerative Medicine
- Dermatology
- Molecular Biology
Background:
- Fibroblast growth factor-7 (FGF-7) normally facilitates cutaneous wound healing.
- Compensatory mechanisms allow normal wound healing in FGF-7-null mice.
- The role of FGF-7 in diabetic wound healing remains to be elucidated.
Purpose of the Study:
- To investigate the impact of FGF-7 deficiency on wound healing in diabetic mice.
- To compare wound healing parameters in FGF-7-null diabetic mice versus diabetic and FGF-7-null controls.
Main Methods:
- Created full-thickness excisional wounds in four groups of mice: FGF-7-null diabetic, FGF-7-null, diabetic, and wild-type.
- Monitored wound closure using digital planimetry.
- Analyzed wound tissues on day 7 via immunohistochemistry (Ki67) and real-time PCR for growth factor expression.
Main Results:
- Diabetic and experimental (FGF-7-null diabetic) groups exhibited significantly delayed wound healing.
- Absence of FGF-7 further exacerbated delayed wound healing in diabetic mice.
- FGF-7 deficiency significantly reduced wound contraction but not epithelialization in diabetic mice.
- Key growth factor expression (TGF-β1, bFGF, EGF) was lower in FGF-7-null diabetic mice compared to diabetic mice.
Conclusions:
- Lack of FGF-7 impairs wound contraction in diabetic mice by altering dermal components.
- FGF-7 does not significantly affect reepithelialization in diabetic wound healing.
- Findings suggest FGF-7-dependent epithelial-mesenchymal interactions are vital for diabetic wound healing.
