title: Lack of FGF-7 further delays cutaneous wound healing in diabetic mice.
abstract: 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.
authors.affiliation: Boston, 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.
authors.forename: Cheng
authors.initials: C
authors.lastname: Peng
authors.forename: Bin
authors.initials: B
authors.lastname: Chen
authors.forename: Huang-Kai
authors.initials: HK
authors.lastname: Kao
authors.forename: George
authors.initials: G
authors.lastname: Murphy
authors.forename: Dennis P
authors.initials: DP
authors.lastname: Orgill
authors.forename: Lifei
authors.initials: L
authors.lastname: Guo
mesh_terms: D000818:Animals; D003433:Crosses, Genetic; D003921:Diabetes Mellitus, Experimental / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D051523:Fibroblast Growth Factor 7 / Q000502:physiology*; D005838:Genotype; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010641:Phenotype; D060888:Real-Time Polymerase Chain Reaction; D012867:Skin / Q000293:injuries* / Q000473:pathology; D014945:Wound Healing / Q000235:genetics* / Q000502:physiology*
chemical_list: C496454:Fgf7 protein, mouse; D051523:Fibroblast Growth Factor 7