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首页> 外文期刊>The FEBS journal >Adipophilin increases triglyceride storage in human macrophages by stimulation of biosynthesis and inhibition of beta-oxidation
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Adipophilin increases triglyceride storage in human macrophages by stimulation of biosynthesis and inhibition of beta-oxidation

机译：脂肪蛋白通过刺激生物合成和抑制β-氧化作用来增加人巨噬细胞中甘油三酸酯的储存

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摘要

Lipid accumulation alters macrophage biology and contributes to lipid retention within the vessel wall. In this study, we investigated the role of adipophilin on triglyceride accumulation and lipid-droplet formation in THP-1-derived macrophages (THP-1 macrophages). In the presence of acetylated low-density lipoprotein, macrophages infected with an adenovirus expressing human adipophilin showed a 31% increase in triglyceride content and a greater number of lipid droplets compared with control cells. Incubation of macrophages with very low-density lipoprotein (VLDL) dramatically increased cellular triglyceride content similarly in control and adipophilin-overexpressing cells. By itself, VLDL increased adipophilin expression, which explains the lack of effect of adipophilin overexpression on cellular triglyceride content in macrophages loaded with VLDL. The lipid-droplet content of macrophages was increased by overexpression of adipophilin and/or loading with VLDL. In contrast, inhibition of adipophilin expression using siRNA prevented lipid-droplet formation and significantly reduced intracellular triglyceride content. Using inhibitors of beta-oxidation and acyl-coenzyme A synthetase, results were obtained which suggest that adipophilin elevates cellular lipids by inhibition of beta-oxidation and stimulation of long-chain fatty acid incorporation into triglycerides. Adipophilin expression in THP-1 macrophages altered the cellular content of different lipids and enhanced the size of lipid droplets, consistent with a role for adipophilin in human foam cell formation.
机译：脂质的积累改变了巨噬细胞的生物学特性，并有助于脂质在血管壁内的滞留。在这项研究中，我们调查了Adipophilin在THP-1衍生的巨噬细胞（THP-1巨噬细胞）中甘油三酸酯积累和脂质滴形成的作用。在存在乙酰化低密度脂蛋白的情况下，与表达对照细胞相比，感染了表达人脂肪蛋白的腺病毒的巨噬细胞的甘油三酸酯含量增加了31％，脂质滴数量增加。巨噬细胞与极低密度脂蛋白（VLDL）的孵育可显着增加对照和过度表达脂肪细胞的细胞中甘油三酸酯的含量。 VLDL本身会增加脂肪蛋白的表达，这解释了脂肪蛋白过表达对负载VLDL的巨噬细胞中细胞甘油三酯含量缺乏影响。巨噬细胞的脂质滴含量通过过高的脂联蛋白表达和/或VLDL负载而增加。相比之下，使用siRNA抑制adipophilin的表达可防止脂质液滴的形成并显着降低细胞内甘油三酯的含量。使用β-氧化和酰基辅酶A合成酶的抑制剂，获得的结果表明，亲脂素通过抑制β-氧化和刺激长链脂肪酸掺入甘油三酸酯来提高细胞脂质。在THP-1巨噬细胞中，adipophilin的表达改变了不同脂质的细胞含量，并增加了脂质液滴的大小，这与adipophilin在人类泡沫细胞形成中的作用一致。

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