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首页> 外文期刊>Life sciences >Effect of simvastatin on Kruppel-like factor2, endothelial nitric oxide synthase and thrombomodulin expression in endothelial cells under shear stress.
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Effect of simvastatin on Kruppel-like factor2, endothelial nitric oxide synthase and thrombomodulin expression in endothelial cells under shear stress.

机译：辛伐他汀对切应力作用下内皮细胞Kruppel-like factor2，内皮型一氧化氮合酶和血栓调节蛋白表达的影响。

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AIMS: Statins (3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors) and fluid wall shear stress have been reported to modulate the expression of genes related to inflammation, blood coagulation, thrombosis, and vascular constriction in cultured endothelial cells. In this study, we investigated the combined effect of laminar shear stress (LSS) and statins on endothelial cell gene expression. MAIN METHODS: Kruppel-like factor 2 (KLF2), endothelial nitric oxide synthase (eNOS), and thrombomodulin (TM) mRNA and protein expression were evaluated in human abdominal aortic endothelial cells (HAAEC) treated with simvastatin (0.1, 1 or 10 microM) at various levels of LSS (0, 1.25, 12.5 or 25 dynes/cm(2)). KEY FINDINGS: As expected, simvastatin and LSS separately enhanced KLF2, eNOS, and TM mRNA expressions. The combination of simvastatin and LSS resulted in significantly higher mRNA levels of all three genes compared to cells treated with LSS only. The highest KLF2, eNOS, and TM mRNA levels were detected at 10 microM simvastatin and 25 dynes/cm(2). Under these conditions, eNOS and TM protein levels were also elevated. Combining LSS and simvastatin produced an overall additive increase in KLF2, eNOS, and TM mRNA. Treatment of the endothelial cells with 10 microM simvastatin and 200 microM mevalonate completely eliminated the effect of simvastatin. SIGNIFICANCE: Our results suggest an additive increase in KLF2, eNOS, and TM expressions when simvastatin and LSS are combined. These results may help to explain the proposed non-lipid lowering benefits of statins observed in the clinic.
机译：目的：据报道，他汀类药物（3-羟基-3-甲基戊二酰辅酶A还原酶抑制剂）和体液壁剪切应力可调节培养的内皮细胞中与炎症，凝血，血栓形成和血管收缩有关的基因的表达。在这项研究中，我们研究了层流切应力（LSS）和他汀类药物对内皮细胞基因表达的联合作用。主要方法：在辛伐他汀（0.1、1或10 microM）处理的人腹主动脉内皮细胞（HAAEC）中评估了Kruppel样因子2（KLF2），内皮一氧化氮合酶（eNOS）和血栓调节蛋白（TM）mRNA和蛋白的表达。 ）在各种LSS水平（0、1.25、12.5或25达因/厘米（2））。主要发现：正如预期的那样，辛伐他汀和LSS分别增强了KLF2，eNOS和TM mRNA的表达。与仅用LSS处理的细胞相比，辛伐他汀和LSS的组合导致所有三个基因的mRNA水平明显升高。在10 microM辛伐他汀和25达因/厘米处检测到最高的KLF2，eNOS和TM mRNA水平（2）。在这些条件下，eNOS和TM蛋白水平也升高。将LSS和辛伐他汀联合使用可使KLF2，eNOS和TM mRNA总体增加。用10 microM辛伐他汀和200 microM甲羟戊酸酯处理内皮细胞完全消除了辛伐他汀的作用。意义：我们的结果表明，当辛伐他汀和LSS联合使用时，KLF2，eNOS和TM表达增加。这些结果可能有助于解释在临床上观察到的他汀类药物的非脂质降低益处。

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