The cell-assisted lipotransfer technique, integrating adipose-derived mesenchymal stem cells (ADMSCs), has transformed lipofilling, enhancing fat graft viability. However, the multipotent nature of ADMSCs poses challenges. To improve safety and graft vitality and to reduce unwanted lineage differentiation, this study refines the methodology by priming ADMSCs into preadipocytes—unipotent, self-renewing cells. We explored the impact of fibroblast growth factor-1 (FGF-1), fibroblast growth factor-2 (FGF-2), and epidermal growth factor (EGF), either alone or in combination, on primary human ADMSCs during the proliferative phase. FGF-2 emerged as a robust stimulator of cell proliferation, preserving stemness markers, especially when combined with EGF. Conversely, FGF-1, while not significantly affecting cell growth, influenced cell morphology, transitioning cells to a rounded shape with reduced CD34 expression. Furthermore, co-priming with FGF-1 and FGF-2 enhanced adipogenic potential, limiting osteogenic and chondrogenic tendencies, and possibly promoting preadipocyte commitment. These preadipocytes exhibited unique features: rounded morphology, reduced CD34, decreased preadipocyte factor 1 (Pref-1), and elevated C/EBPα and PPARγ, alongside sustained stemness markers (CD73, CD90, CD105). Mechanistically, FGF-1 and FGF-2 activated key adipogenic transcription factors—C/EBPα and PPARγ—while inhibiting GATA3 and Notch3, which are adipogenesis inhibitors. These findings hold the potential to advance innovative strategies for ADMSC-mediated lipofilling procedures.

中文翻译：

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FGF-1 和 FGF-2 的优化启动效应增强人脂肪间充质干细胞中的前脂肪细胞谱系定型

细胞辅助脂肪移植技术整合了脂肪来源的间充质干细胞（ADMSC），改变了脂肪填充方式，增强了脂肪移植的活力。然而，ADMSCs 的多能性质带来了挑战。为了提高安全性和移植活力并减少不必要的谱系分化，本研究通过将 ADMSC 启动为前脂肪细胞（单能、自我更新的细胞）来完善方法。我们探讨了成纤维细胞生长因子-1 (FGF-1)、成纤维细胞生长因子-2 (FGF-2) 和表皮生长因子 (EGF) 单独或组合对增殖期原代人 ADMSC 的影响。FGF-2 成为细胞增殖的强大刺激剂，保留干性标记，特别是与 EGF 结合使用时。相反，FGF-1 虽然不会显着影响细胞生长，但会影响细胞形态，使细胞转变为圆形，同时 CD34 表达减少。此外，与 FGF-1 和 FGF-2 共同引发可增强脂肪形成潜力，限制成骨和软骨形成倾向，并可能促进前脂肪细胞定向。这些前脂肪细胞表现出独特的特征：圆形形态、CD34 减少、前脂肪细胞因子 1 (Pref-1) 减少、C/EBPα 和 PPARγ 升高，以及持续的干性标记（CD73、CD90、CD105）。从机制上讲，FGF-1 和 FGF-2 激活关键的脂肪形成转录因子——C/EBPα 和 PPARγ——同时抑制脂肪形成抑制剂 GATA3 和 Notch3。这些发现有可能推动 ADMSC 介导的脂肪填充手术的创新策略。