042 FGF‐BP improves wound healing through the induction of more collagen in rats

Abstract

The fibroblast growth factors are important regulators during wound healing. To quench their biological activities, secreted FGFs are tightly bound to heparan sulfate proteoglycans in the extracellular matrix (ECM). One of the approaches for releasing the active FGF from ECM involves the binding to an FGF binding protein (FGF‐BP), which prevents FGF degradation and retains its activities. FGF‐BP enhances the proliferation of fibroblasts through FGF‐1 and ‐2 and of endothelial cells through FGF‐2. To detect the biological function of FGF‐BP in wound healing, we constructed an adenoviral vector containing murine FGF‐BP cDNA (Ad‐FGF‐BP). Polyvinyl alcohol (PVA) sponges were implanted subcutaneously in rats. 107–108 PFU of either Ad‐FGF‐BP or Ad‐LacZ (as local control) was injected into the sponges at d3 after implantation. At d4 after injection, Ad‐FGF‐BP infected sponges displayed much better organization of granulation tissue with the presence of more macroscopic hemorrhage than the local control. At d7 after injection, Ad‐FGF‐BP infected experimental granulation tissues in sponges showed more collagen deposition. The contents of collagen, protein and DNA in Ad‐FGF‐BP infected sponges increased 24.0%(p < 0.05), 11.3%(p < 0.05, d4) and 28.2%(p < 0.001, d7), respectively. Incisional wounding was performed in rats and 108 PFU Ad‐FGF‐BP or Ad‐lacZ was intracutaneously injected along the wound margins. At 7d after injection, the tensile strength of Ad‐FGF‐BP infected wounds increased 41.1%(p < 0.05). Our data indicate that overexpression of FGF‐BP can improve wound healing, and the inductionof more collagen in granulation tissue may be one of the mechanisms.