Hemizygous deficiency of Krüppel-like factor 2 augments experimental atherosclerosis.
Hemizygous deficiency of Krüppel-like factor 2 augments experimental atherosclerosis.
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DOI：
10.1161/circresaha.108.184663
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发表时间：
2008-09-26
影响因子：
20.1
通讯作者：
Jain MK
中科院分区：
文献类型：
--
作者：
Atkins GB;Wang Y;Mahabeleshwar GH;Shi H;Gao H;Kawanami D;Natesan V;Lin Z;Simon DI;Jain MK
Kruppel样因子2（KLF 2）是体外内皮细胞和单核细胞/巨噬细胞基因表达和功能的核心调节因子。虽然KLF 2在这两种细胞类型中的复合作用预测它可能抑制血管炎症，但KLF 2在体内这一过程中的作用尚未表征。在这项研究中，我们提供的证据表明，半合子缺乏KLF 2增加饮食诱导的动脉粥样硬化载脂蛋白E（ApoE）缺陷小鼠。我们的研究强调了KLF 2在初级巨噬细胞泡沫细胞形成中的重要作用，通过潜在的关键脂质结合蛋白脂肪细胞蛋白2（aP 2）/脂肪酸结合蛋白4（FABP 4）的调节。这些新的观察结果证实KLF 2是一种动脉粥样硬化保护因子。
Kruppel-like factor 2 (KLF2) is a central regulator of endothelial and monocyte/macrophage gene expression and function in vitro. While the composite effects of KLF2 in these two cell types predict that it likely inhibits vascular inflammation, the role of KLF2 in this process in vivo is uncharacterized. In this study, we provide evidence that hemizygous deficiency of KLF2 increased diet-induced atherosclerosis in apolipoprotein E (ApoE) deficient mice. Our studies highlight an important role for KLF2 in primary macrophage foam cell formation via the potential regulation of the key lipid binding protein adipocyte Protein 2 (aP2)/fatty-acid binding protein 4 (FABP4). These novel observations establish that KLF2 is an atheroprotective factor.