KGF Phage Model Peptide Accelerates Cutaneous Wound Healing in a Diabetic Rat Model

Abstract

The authors have previously demonstrated that one phage-displayed keratinocyte growth factor (KGF) model peptide that can bind to epidermal cells and facilitate cellular proliferation. In this study, the authors investigated the role of phage-displayed KGF model peptide on wound healing in diabetic rats. Full-thickness excisional dorsal wounds were created in the diabetic rats, after which the rats were randomly divided into five groups: negative control group [normal saline (NS)], two KGF control groups which were respectively treated with low-dose KGF (5 ng/mL, K-LD) and high-dose KGF (50 ng/mL, K-HD), and two KGF model-peptide-treated groups which were respectively treated with low-dose model peptide (5 ng/mL, M-LD) and high-dose model peptide (50 ng/mL, M-HD). On day 14 post-injury, wound closure was followed by digital planimetry and wound tissues were harvested for histologic assay and real-time polymerase chain reaction. Wounds treated with model peptide closed markedly faster than negative control wounds and were comparable to KGF treated wounds. Histology and immunohistology results demonstrated significantly higher levels of re-epithelization, granulation tissue formation and vascularization in the model peptide groups. Furthermore, real-time polymerase chain reaction expression of KGFR, collagen I and transforming growth factor-β1 in model peptide groups, were also generally higher than that in negative control group. Phage-displayed KGF peptide promotes wound healing through accelerating re-epithelialization, enhancing dermal regeneration, and inducing angiogenesis. Model peptide possesses the potential to be a promising therapeutic option for the treatment of diabetic ulcers.