Funke Sarah, Wiggenhauser Paul Severin, Grundmeier Anna, Fuchs Benedikt, Koban Konstantin, Demmer Wolfram, Giunta Riccardo E, Kuhlmann Constanze
Division of Hand Surgery, Plastic Surgery and Aesthetic Surgery, University Hospital, LMU Munich, Ziemssenstraße 5, 80336 Munich, Germany.
Int J Mol Sci. 2025 Jan 20;26(2):853. doi: 10.3390/ijms26020853.
Aspirin (ASA) is one of the most used medications worldwide and has shown various effects on cellular processes, including stem cell differentiation. However, the effect of ASA on adipogenesis of adipose tissue-derived stem cells (ASCs) remains largely unknown. Considering the potential application of ASCs in regenerative medicine and cell-based therapies, this study investigates the effects of ASA on adipogenic differentiation in human ASCs. ASCs were exposed to varying concentrations of ASA (0 µM, 400 µM, and 1000 µM) and evaluated for changes in morphology, migration, and adipogenic differentiation. While ASA exposure did not affect self-renewal potential, migration ability, or cell morphology, it significantly reduced lipid vacuole formation at 1000 µM after 21 days of adipogenic differentiation ( = 0.0025). This visible inhibition correlated with decreased expression of adipogenic markers (PPARG, ADIPOQ, and FABP4) and the proliferation marker MKi67 under ASA exposure in comparison to the control (ns). Overall, the findings demonstrate that ASA inhibits adipogenic differentiation of human ASCs in a dose-dependent manner in vitro, contrasting its known role in promoting osteogenic differentiation. This research highlights ASA's complex effects on ASCs and emphasizes the need for further investigation into its mechanisms and potential therapeutic applications in obesity and metabolic diseases. The inhibitory effects of ASA on adipogenesis should be considered in cell-based therapies using ASCs.
阿司匹林(ASA)是全球使用最广泛的药物之一,已显示出对细胞过程有多种影响,包括干细胞分化。然而,ASA对脂肪组织来源干细胞(ASC)成脂分化的影响在很大程度上仍不清楚。考虑到ASC在再生医学和基于细胞的治疗中的潜在应用,本研究调查了ASA对人ASC成脂分化的影响。将ASC暴露于不同浓度的ASA(0 μM、400 μM和1000 μM),并评估其形态、迁移和成脂分化的变化。虽然ASA暴露不影响自我更新潜能、迁移能力或细胞形态,但在成脂分化21天后,1000 μM的ASA显著减少了脂滴形成(P = 0.0025)。与对照相比,这种明显的抑制作用与ASA暴露下成脂标志物(PPARG、ADIPOQ和FABP4)以及增殖标志物MKi67的表达降低相关(无显著性差异)。总体而言,研究结果表明,ASA在体外以剂量依赖的方式抑制人ASC的成脂分化,这与其促进成骨分化的已知作用形成对比。本研究突出了ASA对ASC的复杂影响,并强调需要进一步研究其机制以及在肥胖和代谢性疾病中的潜在治疗应用。在使用ASC的基于细胞的治疗中,应考虑ASA对成脂作用的抑制效果。