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Induction of inflammation in vascular endothelial cells by metal oxide nanoparticles: effect of particle composition.

机译:金属氧化物纳米颗粒在血管内皮细胞中诱导炎症:颗粒组成的影响。

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BACKGROUND: The mechanisms governing the correlation between exposure to ultrafine particles and the increased incidence of cardiovascular disease remain unknown. Ultrafine particles appear to cross the pulmonary epithelial barrier into the bloodstream, raising the possibility of direct contact with the vascular endothelium. OBJECTIVES: Because endothelial inflammation is critical for the development of cardiovascular pathology, we hypothesized that direct exposure of human aortic endothelial cells (HAECs) to ultrafine particles induces an inflammatory response and that this response depends on particle composition. METHODS: To test the hypothesis, we incubated HAECs for 1-8 hr with different concentrations (0.001-50 mug/mL) of iron oxide (Fe(2)O(3)), yttrium oxide (Y(2)O(3)), and zinc oxide (ZnO) nanoparticles and subsequently measured mRNA and protein levels of the three inflammatory markers intra-cellular cell adhesion molecule-1, interleukin-8, and monocyte chemotactic protein-1. We also determinednanoparticle interactions with HAECs using inductively coupled plasma mass spectrometry and transmission electron microscopy. RESULTS: Our data indicate that nanoparticle delivery to the HAEC surface and uptake within the cells correlate directly with particle concentration in the cell culture medium. All three types of nanoparticles are internalized into HAECs and are often found within intracellular vesicles. Fe(2)O(3) nanoparticles fail to provoke an inflammatory response in HAECs at any of the concentrations tested; however, Y(2)O(3) and ZnO nanoparticles elicit a pronounced inflammatory response above a threshold concentration of 10 mug/mL. At the highest concentration, ZnO nanoparticles are cytotoxic and lead to considerable cell death. CONCLUSIONS: These results demonstrate that inflammation in HAECs following acute exposure to metal oxide nanoparticles depends on particle composition.
机译:背景:控制超细颗粒暴露与心血管疾病发生率增加之间相关性的机制尚不清楚。超细颗粒似乎穿过肺上皮屏障进入血流,从而增加了与血管内皮直接接触的可能性。目的:由于内皮炎症对于心血管病理的发展至关重要,因此我们假设人主动脉内皮细胞(HAEC)直接暴露于超细颗粒会引起炎症反应,而这种反应取决于颗粒的组成。方法:为了验证该假设,我们将HAEC与不同浓度(0.001-50 cup / mL)的氧化铁(Fe(2)O(3)),氧化钇(Y(2)O(3)孵育1-8小时。 ),氧化锌(ZnO)纳米颗粒,然后测量了三种炎性标记的mRNA和蛋白质水平:细胞内细胞粘附分子1,白介素8和单核细胞趋化蛋白1。我们还使用感应耦合等离子体质谱和透射电子显微镜确定了纳米粒子与HAEC的相互作用。结果:我们的数据表明纳米颗粒向HAEC表面的传递和细胞内的吸收与细胞培养基中的颗粒浓度直接相关。所有这三种类型的纳米颗粒都被内化到HAEC中,并经常在细胞内囊泡中发现。在任何测试浓度下,Fe(2)O(3)纳米颗粒均无法在HAEC中引起炎症反应。然而,Y(2)O(3)和ZnO纳米颗粒在阈值浓度10杯/毫升以上会引起明显的炎症反应。在最高浓度下,ZnO纳米颗粒具有细胞毒性,并导致大量细胞死亡。结论:这些结果表明,急性暴露于金属氧化物纳米颗粒后的HAEC中的炎症取决于颗粒的组成。

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