首页> 美国卫生研究院文献>International Journal of Molecular Sciences >Magnesium Deficiency Induces Lipid Accumulation in Vascular Endothelial Cells via Oxidative Stress—The Potential Contribution of EDF-1 and PPARγ
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Magnesium Deficiency Induces Lipid Accumulation in Vascular Endothelial Cells via Oxidative Stress—The Potential Contribution of EDF-1 and PPARγ

机译:镁缺乏通过氧化应激 - EDF-1和PPARγ的潜在贡献诱导血管内皮细胞中的脂质积累

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摘要

Background: Magnesium deficiency contributes to atherogenesis partly by promoting the dysfunction of endothelial cells, which are critical in vascular homeostasis and diseases. Since EDF-1 and PPARγ regulate crucial endothelial activities, we investigated the modulation of these proteins involved in lipogenesis as well the deposition of lipids in human endothelial cells cultured in different concentrations of magnesium. Methods: Human endothelial cells from the umbilical vein were cultured in medium containing from 0.1 to 5 mM magnesium for 24 h. The levels of EDF-1 and PPARγ were visualized by Western blot. Reactive oxygen species (ROS) were measured by DCFDA. Lipids were detected after O Red Oil staining. Results: Magnesium deficiency leads to the accumulation of ROS which upregulate EDF-1. Further, PPARγ is increased after culture in low magnesium, but independently from ROS. Moreover, lipids accumulate in magnesium-deficient cells. Conclusions: Our results suggest that magnesium deficiency leads to the deposition of lipids by inducing EDF-1 and PPARγ. The increase in intracellular lipids might be interpreted as an adaptive response of endothelial cells to magnesium deficiency.
机译:背景:通过促进内皮细胞的功能障碍,缺乏缺镁对血管生成有助于血管稳态和疾病至关重要。由于EDF-1和PPARγ调节至关重要的内皮活动,我们研究了脂质发生中涉及这些蛋白质的调节,以及在不同浓度的镁培养的人内皮细胞中的沉积。方法:将来自脐静脉的人内皮细胞在含有0.1至5mM镁的培养基中培养24小时。 EDF-1和PPARγ的水平被蛋白质印迹视为可视化。通过DCFDA测量反应性氧物质(ROS)。在红油染色后检测到脂质。结果:缺镁导致ROS的积累,越过EDF-1。此外,在低镁的培养后,PPARγ增加,但独立于ROS。此外,脂质在缺镁细胞中积聚。结论:我们的结果表明,缺镁通过诱导EDF-1和PPARγ来沉积脂质的沉积。细胞内脂质的增加可能被解释为内皮细胞对缺钙的适应性响应。

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