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首页> 外文期刊>Biomaterials >The behavior of endothelial cells on polyurethane nanocomposites and the associated signaling pathways.
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The behavior of endothelial cells on polyurethane nanocomposites and the associated signaling pathways.

机译：聚氨酯纳米复合材料上内皮细胞的行为及其相关的信号通路。

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A series of nanocomposites from polyurethane (PU) incorporated with various low concentrations (17.4-174 ppm) of gold nanoparticles (approximately 5 nm) (denoted PU-Au endothelial cell (EC) migration on biomaterial surfaces. The migration rate of ECs on the PU-Au nanocomposites was determined by a real-time image system. It was found that ECs had the highest migration rate on the nanocomposite containing 43.5 ppm of gold ("PU-Au 43.5 ppm"). The high EC migration rate was associated with increased levels of endothelial nitric oxide synthase (eNOS) and phosphorylated-Akt (p-Akt) expressed by ECs cultured on PU-Au. The inductions of both eNOS and p-Akt on PU-Au were abolished by the addition of LY294002 (PI3K inhibitor), suggesting that these cellular events may be regulated through the PI3K signaling pathway. Using a biotinylated VEGF-165 that recognizes VEGF receptors and by FACS analysis, slightly higher expression of VEGF receptors for ECs on PU-Au was also demonstrated. Phalloidin staining showed that actin appeared as a circumferential band surrounding each cell on tissue culture polystyrene, whereas on PU-Au, especially on PU-Au 43.5 ppm, the cells had their margin spread out and extend processes with stress fibers in the protruding lamellipodia. Moreover, the higher EC migration rate on PU-Au 43.5 ppm was suppressed by LY294002. The higher protein expression of focal adhesion kinase (FAK) on PU-Au 43.5 ppm was observed in FAK-GFP transfected ECs. It was concluded that PU-Au nanocomposites activated FAK and the PI3K/Akt signaling pathway in ECs, leading to proliferation and migration of ECs on these surfaces.
机译：来自聚氨酯（PU）的一系列纳米复合材料，其中掺入了各种低浓度（17.4-174 ppm）的金纳米颗粒（约5 nm）（表示为PU-Au内皮细胞（EC）在生物材料表面上的迁移）。通过实时图像系统测定了PU-Au纳米复合材料，发现ECs在含有43.5 ppm金的纳米复合材料中迁移率最高（“ PU-Au 43.5 ppm”），而EC迁移率较高与通过在PU-Au上培养的EC所表达的内皮一氧化氮合酶（eNOS）和磷酸化Akt（p-Akt）的水平增加。通过添加LY294002（PI3K）可以消除eNOS和p-Akt对PU-Au的诱导抑制剂），表明这些细胞事件可能是通过PI3K信号传导途径调控的。使用可识别VEGF受体的生物素化VEGF-165和通过FACS分析，PU-Au上EC的VEGF受体表达略高。结果表明，肌动蛋白在组织培养聚苯乙烯上以围绕每个细胞的圆周带的形式出现，而在PU-Au上，特别是在43.5 ppm的PU-Au上，细胞的边缘扩散并在凸出的层状脂膜中延伸出应力纤维。此外，LY294002抑制了PU-Au在43.5 ppm上的较高EC迁移速率。在FAK-GFP转染的ECs中观察到PU-Au 43.5 ppm上的粘着斑激酶（FAK）的蛋白质表达较高。结论是，PU-Au纳米复合物激活EC中的FAK和PI3K / Akt信号传导途径，导致EC在这些表面上增殖和迁移。

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