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首页> 外文期刊>Journal of Cellular Physiology >In Type 2 Diabetes Mellitus Glycated Albumin Alters Macrophage Gene Expression Impairing ABCA1-Mediated Cholesterol Efflux
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In Type 2 Diabetes Mellitus Glycated Albumin Alters Macrophage Gene Expression Impairing ABCA1-Mediated Cholesterol Efflux

机译：在2型糖尿病糖化白蛋白改变巨噬细胞基因表达的影响ABCA1-Mediated胆固醇流出

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Advanced glycation end products (AGE) are elevated in diabetes mellitus (DM) and predict the development of atherosclerosis. AGE-albumin induces oxidative stress, which is linked to a reduction in ABCA-1 and cholesterol efflux. We characterized the glycation level of human serum albumin (HSA) isolated from poorly controlled DM2 (n=11) patients compared with that of control (C, n=12) individuals and determined the mechanism by which DM2-HSA can interfere in macrophage lipid accumulation. The HSA glycation level was analyzed by MALDI/MS. Macrophages were treated for 18h with C- or DM2-HSA to measure the C-14-cholesterol efflux, the intracellular lipid accumulation and the cellular ABCA-1 protein content. Agilent arrays (44000 probes) were used to analyze gene expression, and the differentially expressed genes were validated by real-time RT-PCR. An increased mean mass was observed in DM2-HSA compared with C-HSA, reflecting the condensation of at least 5 units of glucose. The cholesterol efflux mediated by apo AI, HDL3, and HDL2 was impaired in DM2-HSA-treated cells, which was related to greater intracellular lipid accumulation. DM2-HSA decreased Abcg1 mRNA expression by 26%. Abca1 mRNA was unchanged, although the final ABCA-1 protein content decreased. Compared with C-HAS-treated cells, NADPH oxidase 4 mRNA expression increased in cells after DM2-HSA treatment. Stearoyl-Coenzyme A desaturase 1, janus kinase 2, and low density lipoprotein receptor mRNAs were reduced by DM2-HSA. The level of glycation that occurs in vivo in DM2-HSA-treated cells selectively alters macrophage gene expression, impairing cholesterol efflux and eliciting intracellular lipid accumulation, which contribute to atherogenesis, in individuals with DM2. J. Cell. Physiol. XXXX: XX-XX, 2015. (c) 2015 Wiley Periodicals, Inc. J. Cell. Physiol. 230: 1250-1257, 2015. (c) 2014 Wiley Periodicals, Inc., A Wiley Company
机译：高级糖化终端产品(年龄)升高在糖尿病(DM)和预测动脉粥样硬化的发展。诱发氧化应激,这是连接到一个减少ABCA-1和胆固醇流出。人类血清糖化水平的特征白蛋白(HSA)隔绝DM2控制不好(n = 11)患者与控制(C,n = 12)个人和决定的机制DM2-HSA可以干涉巨噬细胞脂质积累。分析了MALDI /女士。18 h和C -或DM2-HSA测量C-14-cholesterol流出,细胞内脂质积累和细胞ABCA-1蛋白质内容。分析基因表达,差异表达基因进行验证实时rt - pcr。观察到DM2-HSA与C-HSA相比,反映至少5单位的凝结的葡萄糖。apo AI, HDL3, HDL2受损DM2-HSA-treated细胞,这是相关的更大的细胞内脂质积聚。Abcg1 mRNA表达下降了26%。信使rna持平,尽管最后ABCA-1蛋白质含量下降。C-HAS-treated细胞NADPH氧化酶4 mRNADM2-HSA后细胞中表达增加治疗。janus激酶2,低密度脂蛋白受体信使rna被DM2-HSA减少。发生在体内的糖化DM2-HSA-treated细胞选择性的改变巨噬细胞基因表达,降低胆固醇射流和诱发细胞内脂质导致动脉粥样化形成积累,与DM2个人。XX-XX, 2015年。细胞。威利期刊,Inc .威利公司

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