HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

Lack of FGF-7 further delays cutaneous wound healing in diabetic mice.

AbstractBACKGROUND:
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.
AuthorsCheng Peng, Bin Chen, Huang-Kai Kao, George Murphy, Dennis P Orgill, Lifei Guo
JournalPlastic and reconstructive surgery (Plast Reconstr Surg) Vol. 128 Issue 6 Pg. 673e-684e (Dec 2011) ISSN: 1529-4242 [Electronic] United States
PMID22094769 (Publication Type: Journal Article)
Chemical References
  • Fgf7 protein, mouse
  • Fibroblast Growth Factor 7
Topics
  • Animals
  • Crosses, Genetic
  • Diabetes Mellitus, Experimental (genetics, pathology, physiopathology)
  • Female
  • Fibroblast Growth Factor 7 (physiology)
  • Genotype
  • Male
  • Mice
  • Mice, Inbred Strains
  • Phenotype
  • Real-Time Polymerase Chain Reaction
  • Skin (injuries, pathology)
  • Wound Healing (genetics, physiology)

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: