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首页> 外文期刊>Scientific reports. >The interleukin-33-mediated inhibition of expression of two key genes implicated in atherosclerosis in human macrophages requires MAP kinase, phosphoinositide 3-kinase and nuclear factor-κB signaling pathways
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The interleukin-33-mediated inhibition of expression of two key genes implicated in atherosclerosis in human macrophages requires MAP kinase, phosphoinositide 3-kinase and nuclear factor-κB signaling pathways

机译：白细胞介素-33-介导的两个关键基因表达的抑制涉及人类巨噬细胞的动脉粥样硬化需要MAP激酶，磷酸膦酸3-激酶和核因子-κB信号传导途径

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Atherosclerosis, a chronic inflammatory disorder of the walls of arteries, causes more deaths worldwide than any other disease. Cytokines, which are present at high levels in atherosclerotic plaques, play important roles in regulating the initiation and the progression of the disease. Previous studies using animal and cell culture model systems revealed protective, anti-atherogenic effects of the cytokine interleukin-33 (IL-33). The action of this cytokine involves both the induction and suppression of expression of many genes. Unfortunately, the signaling pathways that are responsible for the inhibition of gene expression by this cytokine are poorly understood. Further studies are required given the important roles of genes whose expression is inhibited by IL-33 in key cellular processes associated with atherosclerosis such as monocyte recruitment, foam cell formation and lipoprotein metabolism. We have investigated here the roles of various known IL-33 activated signaling pathways in such inhibitory actions using RNA interference-mediated knockdown assays and monocyte chemotactic protein-1 and intercellular adhesion molecule-1 as model genes. Key roles were identified for extracellular signal-regulated kinase-1/2, p38α kinase, c-Jun N-terminal kinase-1/2, phosphoinositide 3-kinase-γ, and p50 and p65 nuclear factor-κB in such inhibitory action of IL-33. These studies provide new insights on the signaling pathways through which IL-33 inhibits the macrophage expression of key atherosclerosis-associated genes.
机译：动脉粥样硬化，动脉壁的慢性炎症疾病，导致全世界的死亡更多，而不是任何其他疾病。在动脉粥样硬化斑块的高水平存在的细胞因子，在调节疾病的开始和进展方面起着重要作用。以前使用动物和细胞培养模型系统的研究揭示了细胞因子白细胞介素-33（IL-33）的保护性，抗动脉粥样硬化作用。这种细胞因子的作用涉及许多基因表达的诱导和抑制。遗憾的是，负责该细胞因子抑制基因表达的信号传导途径很差。鉴于在与动脉粥样硬化如单核细胞募集，泡沫细胞形成和脂蛋白代谢如单核细胞屈曲，泡沫细胞形成和脂蛋白代谢相关的关键细胞过程中，鉴于IL-33抑制的基因的重要作用，需要进一步的研究。这里我们研究了各种已知的IL-33活化信号传导途径在这种抑制作用中使用RNA干扰介导的敲击测定和单核细胞趋化蛋白-1和细胞间粘附分子-1作为模拟基因的抑制作用。用于细胞外信号调节的激酶-1 / 2，P38α激酶，C-JUN N-末端激酶-1 / 2，P50和P65核因子-κB的关键作用在这种抑制作用中IL-33。这些研究对信号通路提供了新的见解，IL-33抑制关键动脉粥样硬化相关基因的巨噬细胞表达。

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