BACKGROUND: Platelet-rich fibrin (PRF) can promote fat graft survival, but limited data are currently available, and the underlying mechanism of this effect has not yet been explained. OBJECTIVES: The aim of this study was to explore the mechanism by which PRF promotes fat graft survival, from the aspects of angiogenesis, adipogenesis, cellular apoptosis, and collagen production. METHODS: Nude mice were randomly assigned to a PRF group (subcutaneously injected with PRF and fat in the ratio of 1:5 by volume) and a control group (subcutaneously injected with normal saline and fat in the ratio of 1:5 by volume). On days 0, 3, 7, 14, 21, and 28 after transplantation, graft samples (n = 12) were obtained for quantification of target growth factors. In weeks 1, 2, 3, and 4 after transplantation, graft samples (n = 12) were obtained for the following evaluations. The volume and weight retention rates were calculated; gene and protein expression of vascular endothelial growth factor A (VEGF-A), peroxisome proliferator-activated receptor γ (PPAR-γ), COL1-A1, and BAX were evaluated; hematoxylin & eosin staining, Masson's trichrome staining, α smooth muscle actin staining, and perilipin-1 staining were performed to evaluate graft survival. RESULTS: After transplantation, the concentrations of growth factors produced by the fat increased to varying degrees, and the addition of PRF made these concentration changes ever greater. Compared with the control group, the PRF group had a higher volume and weight retention rate, a higher expression level of VEGF-A and PPAR-γ, a lower expression level of COL1-A1 and BAX, a higher vessel density, less fibrosis, and more viable adipocytes. CONCLUSIONS: PRF can promote autocrine function of the grafted fat to produce more growth factors. It greatly increased fat retention rate, possibly by promoting vascularization and adipogenic differentiation, inhibiting cellular apoptosis, and regulating collagen production.
BACKGROUND: Platelet-rich fibrin (PRF) can promote fat graft survival, but limited data are currently available, and the underlying mechanism of this effect has not yet been explained. OBJECTIVES: The aim of this study was to explore the mechanism by which PRF promotes fat graft survival, from the aspects of angiogenesis, adipogenesis, cellular apoptosis, and collagen production. METHODS:Nude mice were randomly assigned to a PRF group (subcutaneously injected with PRF and fat in the ratio of 1:5 by volume) and a control group (subcutaneously injected with normal saline and fat in the ratio of 1:5 by volume). On days 0, 3, 7, 14, 21, and 28 after transplantation, graft samples (n = 12) were obtained for quantification of target growth factors. In weeks 1, 2, 3, and 4 after transplantation, graft samples (n = 12) were obtained for the following evaluations. The volume and weight retention rates were calculated; gene and protein expression of vascular endothelial growth factor A (VEGF-A), peroxisome proliferator-activated receptor γ (PPAR-γ), COL1-A1, and BAX were evaluated; hematoxylin & eosin staining, Masson's trichrome staining, α smooth muscle actin staining, and perilipin-1 staining were performed to evaluate graft survival. RESULTS: After transplantation, the concentrations of growth factors produced by the fat increased to varying degrees, and the addition of PRF made these concentration changes ever greater. Compared with the control group, the PRF group had a higher volume and weight retention rate, a higher expression level of VEGF-A and PPAR-γ, a lower expression level of COL1-A1 and BAX, a higher vessel density, less fibrosis, and more viable adipocytes. CONCLUSIONS: PRF can promote autocrine function of the grafted fat to produce more growth factors. It greatly increased fat retention rate, possibly by promoting vascularization and adipogenic differentiation, inhibiting cellular apoptosis, and regulating collagen production.