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首页> 外文期刊>Cell biology international. >miR-497 accelerates oxidized low-density lipoprotein-induced lipid accumulation in macrophages by repressing the expression of apelin
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miR-497 accelerates oxidized low-density lipoprotein-induced lipid accumulation in macrophages by repressing the expression of apelin

机译：MiR-497通过抑制阿比松表达，加速氧化低密度脂蛋白诱导的巨噬细胞脂质积累

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microRNAs (miRNAs) play important roles in the pathogenesis of atherosclerosis. A previous study has reported that miR-497 is elevated in advanced atherosclerotic lesions in an apoE-deficient (apoE-/-) mouse model. The purpose of this study is to test whether miR-497 can modulate macrophage foam cell formation, an initiating event in atherosclerosis. We found that miR-497 was upregulated in THP-1 macrophages after treatment with oxidized low-density lipoprotein (oxLDL). Enforced expression of miR-497 promoted lipid accumulation and decreased cholesterol efflux in oxLDL-exposed THP-1 macrophages. In contrast, downregulation of miR-497 suppressed oxLDL-induced lipid accumulation in THP-1 macrophages. Apelin was identified to be a downstream target of miR-497. Overexpression of miR-497 significantly reduced the expression of apelin in THP-1 macrophages. Interestingly, delivery of a miR-497-resistant variant of apelin significantly inhibited lipid accumulation and enhanced cholesterol efflux in miR-497-overexpressing THP-1 macrophages in response to oxLDL. In addition, miR-497 expression was increased and negatively correlated with apelin protein expression in human atherosclerotic lesions. In conclusion, miR-497 contributes to oxLDL-induced lipid deposition in macrophages largely via targeting of apelin and thus represents a potential therapeutic target for atherosclerosis.
机译：microRNA（miRNA）在动脉粥样硬化的发病机制中起着重要作用。之前的一项研究报道，在apoE缺陷（apoE-/-）小鼠模型中，miR-497在晚期动脉粥样硬化病变中升高。本研究的目的是检测miR-497是否可以调节巨噬细胞泡沫细胞的形成，这是动脉粥样硬化的始发事件。我们发现，经氧化低密度脂蛋白（oxLDL）处理后，THP-1巨噬细胞中的miR-497表达上调。miR-497的强制表达促进氧化低密度脂蛋白暴露的THP-1巨噬细胞中的脂质积累并减少胆固醇流出。相反，miR-497的下调抑制了氧化低密度脂蛋白诱导的THP-1巨噬细胞中的脂质积聚。Apelin被确定为miR-497的下游靶点。miR-497的过度表达显著降低了THP-1巨噬细胞中apelin的表达。有趣的是，在miR-497过度表达的THP-1巨噬细胞中，输送具有miR-497抗性的apelin变体可显著抑制脂质积聚并增强胆固醇流出，从而对oxLDL产生应答。此外，在人类动脉粥样硬化病变中，miR-497表达增加，并与apelin蛋白表达呈负相关。总之，miR-497主要通过靶向apelin参与oxLDL诱导的巨噬细胞脂质沉积，因此是动脉粥样硬化的潜在治疗靶点。

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