Mechanism of acceleration of wound healing by basic fibroblast growth factor in genetically diabetic mice.

To elucidate the role of basic fibroblast growth factor (bFGF) in the wound healing process, we investigated the ability of the factor to modulate an inflammatory reaction at the wound site and to influence endothelial cells and fibroblasts in vitro. A single, topical application of bFGF to a full-thickness wound of genetically diabetic mice caused an increase in the volume of wound exudate in a dose-dependent manner. bFGF induced the infiltration of a large number of leukocytes in the wound exudate. Transforming growth factor-beta (TGF-beta) positive cells, such as macrophages, monocytes and fibroblasts, appeared in the granulation tissue in bFGF-treated diabetic mice. These phenomena were comparable to those in normal animals, suggesting that the treatment with bFGF restored the inflammatory response in wound healing of diabetic mice. The effects of bFGF on cell proliferation, migration and angiogenesis were histologically recognized as shown in enhanced granulation tissue formation and neovascularization. It is suggested that bFGF promotes the recruitment of inflammatory cells into the wound site to induce a cascade reaction of growth factors including TGF-beta in a wound healing process, and so would accelerate wound healing.