PRF Extract Suppresses TGF-β1-Induced Fibrosis in Schneiderian Membrane Healing

Objectives: TGF-β1, concentrated in platelet-rich fibrin (PRF), plays a crucial role in promoting tissue fibrosis by increasing the production of extracellular matrix (ECM). Here, we investigated the effect of PRF on perforated Schneiderian membrane (SM) and the role of TGF-β1 in rabbit Schneiderian membrane-derived cells (rSMDCs).
Methods: We assessed the effect of PRF on histological repair in a rabbit Schneiderian membrane perforation model. rSMDCs were extracted and identified before being treated with PRF extract and/or 20 ng/ml TGF-β1. Then, morphological changes, cell proliferation and migration were observed with a light microscope and CCK-8, while expression levels of markers of fibroblast-myofibroblast transition (FMT) and cananical TGF-β signaling pathway were evaluated with qRT-PCR and western blot.
Results: PRF reduced collagen deposition (control vs PRF = 34.31±7.37 % vs 27.61±4.53 %) in the lamina propria of SM and significantly restored the number of serous glands (6.00±4.36 vs 32.00±4.64) in vivo. rSMDCs showed more prominent proliferation (control vs 3d PRF vs 7d PRF = 0.33±0.03 vs 0.71±0.07 vs 0.54±0.04) and migration (212.22±49.04 μm vs 397.38±44.11 μm vs 397.72±30.69 μm
) in the PRF-treated group. The FMT markers (collagen Ι and α-SMA) and markers of cananical TGF-β signaling pathway were promoted in the TGF-β1-treated group, while these changes were reversed by cotreatment with PRF extract.
Conclusions: PRF extract reversed the trends of FMT induced by TGF-β1 in rSMDCs, which might be associated with suppressed cananical TGF-β signaling pathway, indicating a potential for applying PRF to reduce tissue fibrosis.