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and TGF-
in the Skin Wound-Healing Process1
* Division of Molecular Bioregulation, Cancer Research Institute, Kanazawa University, Kanazawa, Japan;
Department of Legal Medicine, Wakayama Medical University, Wakayama, Japan;
Department of Forensic and Social Environmental Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan; and
Laboratory Animal Research Center, Institute of Medical Science, University of Tokyo, Tokyo, Japan
Several lines of in vitro evidence suggest the potential role of IFN-
in angiogenesis and collagen deposition, two crucial steps in the wound healing process. In this report, we examined the role of IFN- in the skin wound healing process utilizing WT and IFN- KO mice. In WT mice, excisional wounding induced IFN- mRNA and protein expression by infiltrating macrophages and T cells, with a concomitant enhancement of IL-12 and IL-18 gene expression. Compared with WT mice, IFN- KO mice exhibited an accelerated wound healing as evidenced by rapid wound closure and granulation tissue formation. Moreover, IFN- KO mice exhibited enhanced angiogenesis with augmented vascular endothelial growth factor mRNA expression in wound sites, compared with WT mice, despite a reduction in the infiltrating neutrophils, macrophages, and T cells. IFN- KO mice also exhibited accelerated collagen deposition with enhanced production of TGF-
1 protein in wound sites, compared with WT mice. Furthermore, the absence of IFN- augmented the TGF-1-mediated signaling pathway, as evidenced by increases in the levels of total and phosphorylated Smad2 and a reciprocal decrease in the levels of Smad7. These results demonstrate that there is crosstalk between the IFN-/Stat1 and TGF-1/Smad signaling pathways in the wound healing process.
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