Research Article

载脂蛋白A5和人类脂肪间充质干细胞成脂调控的新见解。

卷 20, 期 2, 2020

页: [144 - 156] 页: 13

弟呕挨: 10.2174/1566524019666190927155702

价格: $65

摘要

背景:肥胖症的标志是甘油三酸酯(TG)在脂肪组织中的过度积累。载脂蛋白A5(ApoA5)已显示影响肥胖症的患病率和发病机理。但是,基本机制仍有待阐明。 方法:用600 ng / ml人重组ApoA5蛋白处理人脂肪来源的间充质干细胞(AMSC)。确定了ApoA5对细胞内TG含量和成脂相关因子表达的影响。此外,还观察到ApoA5对CIDE-C表达的影响。 结果:在脂肪形成过程中,ApoA5处理可减少脂质滴的细胞内积累和TG水平。同时,ApoA5下调了脂肪形成相关因子的表达水平,包括CCAAT增强子结合蛋白α/β(C /EBPα/β),脂肪酸合成酶(FAS)和脂肪酸结合蛋白4(FABP4)。此外,通过抑制CIDE-C表达来介导ApoA5对脂肪形成的抑制,CIDE-C表达是促进脂肪形成过程的重要因素。但是,过度表达细胞内CIDE-C可能会导致ApoA5在抑制AMSCs成脂中的功能丧失。 结论:总之,ApoA5通过至少部分下调CIDE-C表达来抑制AMSC的成脂过程。本研究提供了新颖的机制,通过该机制,ApoA5可通过人类的AMSC预防肥胖。

关键词: 载脂蛋白A5,CIDE-C,脂肪来源的间充质干细胞,脂肪形成,抑制,AMSC

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