C反应蛋白和高密度脂蛋白对血凝素样氧化型低密度脂蛋白受体1表达的影响
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C-Reactive Protein and High Density Lipoprotein Promote Lectin-Like Oxidized Low Density Lipoprotein Receptor-1 Expression on THP-1 Derived Macrophages
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    摘要:

    目的观察C反应蛋白和高密度脂蛋白对单核细胞株THP-1来源的巨噬细胞血凝素样氧化型低密度脂蛋白受体1蛋白和mRNA表达的影响,以及血凝素样氧化型低密度脂蛋白受体1表达的变化与细胞内胆固醇含量变化的关系。方法THP-1单核细胞株经佛波酯诱导分化为巨噬细胞。用不同浓度C反应蛋白或高密度脂蛋白在体外干预巨噬细胞,测定干预前后巨噬细胞血凝素样氧化型低密度脂蛋白受体1蛋白和mRNA表达的变化,并采用高效液相色谱测定巨噬细胞内胆固醇含量的变化。结果与对照组相比,C反应蛋白或高密度脂蛋白均可以诱导THP-1来源的巨噬细胞血凝素样氧化型低密度脂蛋白受体1蛋白和mRNA表达增加(P<0.05),C反应蛋白使巨噬细胞内总胆固醇和胆固醇酯含量显著增加(P<0.01),而高密度脂蛋白使细胞内总胆固醇和胆固醇酯显著降低(P<0.01)。结论C反应蛋白和高密度脂蛋白都能引起THP-1来源的巨噬细胞表面血凝素样氧化型低密度脂蛋白受体1表达上调,提示血凝素样氧化型低密度脂蛋白受体1并不是介导巨噬细胞参与炎症反应病理生理变化的关键性受体。

    Abstract:

    Aim To investigate the role of macrophage lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) in the process of atherosclerosis inflammation, the effects of C-reactive protein (CRP) or high density lipoprotein (HDL) on LOX-1 mRNA and protein expression, and on intracellular cholesterol content in THP-1 derived macrophages were investigated. Methods THP-1 cells were differentiated into macrophages with PMA. THP-1 derived macrophages were incubated with CRP or HDL of different concentration in vitro. The expressions of LOX-1 antigen and mRNA were determined by ELISA and RT-PCR. Cellular cholesterol contents were measured before and after CRP or HDL treatments with HPLC. Results Compared with control group, both CRP and HDL can increase the expression of LOX-1 protein and mRNA significantly (P<0.05) in a dose dependent manner on THP-1 derived macrophages. CRP promoted cellular cholesterol accumulation (P<0.01), while HDL decreased intracellular cholesterol content significantly (P<0.01). Conclusions LOX-1 expression in THP-1 derived macrophages can be promoted by either pro-inflammatory factor CRP or anti-inflammatory factor HDL, which suggested that LOX-1 may not play a critical role in the inflammatory process of macrophages.

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王悦,陈连凤,王晋峰,方全,严晓伟. C反应蛋白和高密度脂蛋白对血凝素样氧化型低密度脂蛋白受体1表达的影响[J].中国动脉硬化杂志,2008,16(2):129~131.

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  • 收稿日期:2007-08-13
  • 最后修改日期:2008-01-02
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