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首页> 外文期刊>Cell and Tissue Research >High-fat diet alters protein composition of detergent-resistant membrane microdomains
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High-fat diet alters protein composition of detergent-resistant membrane microdomains

机译：高脂饮食改变耐洗涤剂膜微区的蛋白质组成

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A high-lipid diet is one of the main risk factors in atherosclerosis and can induce changes in the composition of plasma membrane microdomains. In response, important functions such as vesicle trafficking, protein docking, signaling and receptor recognition are significantly altered. In particular, interactions of heat-shock proteins (Hsps), acting as danger signals, with components of the membrane microdomains can influence signaling pathways and the inflammatory response of cells. Our study focuses on the composition of detergent-resistant membrane (DRM) isolated from ApoE-/- mice fed a standard or high-fat diet with and without fluvastatin treatment versus appropriate controls. Biochemical studies, immunoblotting and liquid chromatography mass spectrometric analysis were performed to investigate whether the structural components (such as caveolin and cavin) of the detergent-resistant microdomains were correlated with the expression and secretion of stress-inducible Hsps (Hsp70 and Hsp90) and AKT phosphorylation in experimental atherosclerosis. ApoE-/- mice challenged with a high-fat diet developed extensive atherosclerotic plaques in lesion-prone areas. DRM harvested from hyperlipidemic animals showed a modified biochemical composition with cholesterol, glycerolipids, caveolin-1 and phospho-AKT being up-regulated, whereas cavin-1 and dynamin were down-regulated. The data also demonstrated the co-fractionation of Hsps with caveolin-1 in isolated DRM, expression being positively correlated with their secretion into blood serum. Statin therapy significantly attenuated the processes induced by the development of atherosclerosis in ApoE-/- mice under a high-fat diet. Thus, high-lipid stress induces profound changes in DRM biochemistry and modifies the cellular response, supporting the systemic inflammatory onset of atherosclerosis.
机译：高脂饮食是动脉粥样硬化的主要危险因素之一，可诱发质膜微区组成的变化。作为响应，诸如囊泡运输，蛋白质对接，信号传导和受体识别的重要功能被显着改变。特别是，作为危险信号的热休克蛋白（Hsps）与膜微区的组成部分之间的相互作用会影响信号传导途径和细胞的炎症反应。我们的研究重点是从饲喂标准或高脂饮食（加或不加氟伐他汀治疗）的ApoE-/-小鼠中分离的耐洗涤剂膜（DRM）的组成，以及适当的对照。进行了生化研究，免疫印迹和液相色谱质谱分析，以研究耐去污剂的微区的结构成分（例如小窝蛋白和cavin）是否与应激诱导的Hsps（Hsp70和Hsp90）和AKT的表达和分泌相关。实验性动脉粥样硬化中的磷酸化。受到高脂饮食挑战的ApoE-/-小鼠在容易发生病变的区域形成了广泛的动脉粥样硬化斑块。从高脂血症动物中收获的DRM显示出经过修饰的生化成分，其中胆固醇，甘油脂，小窝蛋白1和磷酸化AKT上调，而cavin-1和dynamin则下调。数据还证明了Hsps与caveolin-1在分离的DRM中的共同分离，表达与其在血清中的分泌呈正相关。他汀类药物疗法可显着减轻高脂饮食对ApoE-/-小鼠动脉粥样硬化发展的诱导过程。因此，高脂应激可引起DRM生物化学的深刻变化并改变细胞反应，从而支持动脉粥样硬化的全身性炎症发作。

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