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Establishment of a lipid accumulation model in an insect cell line

机译:昆虫细胞系脂质积累模型的建立

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The study of adipocyte differentiation and lipid accumulation in insects has been limited by the lack of a system suitable for analysis of molecular mechanisms. Here, we describe the establishment of a model system of lipid accumulation in BmN4 cells, which are derived from silkworm ovary. In BmN4 cells, dexamethasone treatment induced accumulation of lipid, suppressed cellular proliferation, and caused the cells to form aggregates. We isolated the Bombyx mori fatty acid binding protein 1 gene (BmFABP1), which is the silkworm homologue of mouse Fabp4 (aP2), a marker of adipocyte differentiation in mammals. BmFABP1 expression was increased by dexamethasone treatment. We also isolated the BmFABP1 promoter, and found that it was activated by a combination of drugs that included dexamethasone. The demonstration of dexamethasone-stimulated lipid accumulation and BmFABP1 expression in BmN4 cells provides a useful model of inducible adipogenesis. This system should be valuable for investigation of the molecular mechanisms of fat body formation, adipocyte differentiation, and lipid accumulation in the silkworm and other Lepidopteran insects.
机译:昆虫中脂肪细胞分化和脂质积累的研究由于缺乏适合分子机理分析的系统而受到限制。在这里,我们描述了从家蚕卵巢衍生的BmN4细胞中脂质蓄积的模型系统的建立。在BmN4细胞中,地塞米松治疗诱导脂质蓄积,抑制细胞增殖,并导致细胞形成聚集体。我们分离出家蚕脂肪酸结合蛋白1基因(BmFABP1),它是小鼠Fabp4(aP2)(哺乳动物脂肪细胞分化的标志物)的家蚕同源物。地塞米松处理可增加BmFABP1的表达。我们还分离了BmFABP1启动子,并发现它被包括地塞米松在内的多种药物激活。地塞米松刺激的脂质蓄积和BmN4细胞中BmFABP1表达的演示提供了诱导脂肪形成的有用模型。该系统对于研究家蚕和其他鳞翅目昆虫中脂肪体形成,脂肪细胞分化和脂质蓄积的分子机制是有价值的。

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