Advanced platelet-rich fibrin promotes the paracrine function and proliferation of adipose-derived stem cells and contributes to micro-autologous fat transplantation by modulating and .

Background: The micro-autologous fat transplantation (MAFT) technique has demonstrated its feasibility in multiple medical fields, such as facial rejuvenation. Advanced platelet-rich fibrin (), an autologous platelet concentrated on a fibrin membrane without added external factors, has shown significant potential for tissue restoration. However, the role of in the modulation of MAFT remains unclear. Here, we aimed to explore the effect of on MAFT.

Methods: Adipose-derived stem cells (ASCs) were isolated from human gastric subcutaneous fat and treated with . ELISA assays measured cytokines. The proliferation of ASCs was analyzed by CCK-8 assays. The levels of hypoxia-inducible factor-1α (), heat shock protein 70 (), insulin like growth factor 2 (), interleukin-6 (), interleukin-8 (), and vascular endothelial growth factor () were measured by ELISA assays, quantitative reverse transcription-PCR (qRT-PCR), and Western blot analysis. The effect of // on MAFT was analyzed in Balb/c nude mice. The BALB/c mice were subcutaneously co-transplanted with fat, , and control shRNA, shRNA, or shRNA into the dorsal area. The serum and protein levels of the above cytokines were analyzed by ELISA assays and Western blot analysis. Lipid accumulation was measured by Oil Red O staining. The expression of CD34 was assessed by immunohistochemical staining.

Results: continuously secreted multiple cytokines, including epidermal growth factor (), FGF-2, insulin like growth factor 1 (), interleukin-1beta (), interleukin-4 (), platelet-derived growth factor alpha polypeptide b (), platelet-derived growth factor beta polypeptide b (), transforming growth factor-beta (), and . was able to promote the proliferation of ASCs. dose-dependently activated the expression of , , , , , and in ASCs. regulated the paracrine function of ASCs by modulating and increased the survival of MAFT by modulating and .

Conclusions: promotes the paracrine function and proliferation of ASCs and contributes to MAFT by modulating and . Our findings provide new insights into the mechanism by which regulates MAFT.