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首页> 外文期刊>Nanotechnology >Fe2O3 nanoparticles suppress Kv1.3 channels via affecting the redox activity of Kv beta 2 subunit in Jurkat T cells
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Fe2O3 nanoparticles suppress Kv1.3 channels via affecting the redox activity of Kv beta 2 subunit in Jurkat T cells

机译：Fe2O3纳米颗粒通过影响Jurkat T细胞中Kv beta 2亚基的氧化还原活性来抑制Kv1.3通道

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Superparamagnetic iron oxide nanoparticles (SPIONs) are promising nanomaterials in medical practice due to their special magnetic characteristics and nanoscale size. However, their potential impacts on immune cells are not well documented. This study aims to investigate the effects of Fe2O3 nanoparticles (Fe2O3-NPs) on the electrophysiology of Kv1.3 channels in Jurkat T cells. Using the whole-cell patch-clamp technique, we demonstrate that incubation of Jurkat cells with Fe2O3-NPs dose-and time-dependently decreased the current density and shifted the steady-state inactivation curve and the recovery curve of Kv1.3 channels to a rightward direction. Fe2O3-NPs increased the NADP level but decreased the NADPH level of Jurkat cells. Direct induction of NADPH into the cytosole of Jurkat cells via the pipette abolished the rightward shift of the inactivation curve. In addition, transmission electron microscopy showed that Fe2O3-NPs could be endocytosed by Jurkat cells with relatively low speed and capacity. Fe2O3-NPs did not significantly affect the viability of Jurkat cells, but suppressed the expressions of certain cytokines (TNF alpha, IFN gamma and IL-2) and interferon responsive genes (IRF-1 and PIM-1), and the time courses of Fe2O3-NPs endocytosis and effects on the expressions of cytokines and interferon responsive genes were compatible. We conclude that Fe2O3-NPs can be endocytosed by Jurkat cells and act intracellularly. Fe2O3-NPs decrease the current density and delay the inactivation and recovery kinetics of Kv1.3 channels in Jurkat cells by oxidizing NADPH and therefore disrupting the redox activity of the Kv beta 2 auxiliary subunit, and as a result, lead to changes of the Kv1.3 channel function. These results suggest that iron oxide nanoparticles may affect T cell function by disturbing the activity of Kv1.3 channels. Further, the suppressing effects of Fe2O3-NPs on the expressions of certain inflammatory cytokines and interferon responsive genes suggest that iron oxide nanoparticles may exert modulatory effects on T cell immune activities and anti-inflammation effects.
机译：超顺磁性氧化铁纳米粒子（SPIONs）由于其特殊的磁性和纳米级尺寸，在医学实践中是很有前途的纳米材料。但是，它们对免疫细胞的潜在影响尚未得到充分证明。这项研究旨在调查Fe2O3纳米颗粒（Fe2O3-NPs）对Jurkat T细胞中Kv1.3通道电生理的影响。使用全细胞膜片钳技术，我们证明了Jurkat细胞与Fe2O3-NPs的剂量依赖性和时间依赖性孵育会降低电流密度，并将稳态灭活曲线和Kv1.3通道的恢复曲线转移至向右的方向。 Fe2O3-NPs增加了Jurkat细胞的NADP水平，但降低了NADPH水平。通过移液管将NADPH直接诱导入Jurkat细胞的细胞底，消除了失活曲线的向右移动。此外，透射电子显微镜显示Fe2O3-NPs可以被Jurkat细胞内吞，且速度和容量较低。 Fe2O3-NPs不会显着影响Jurkat细胞的生存能力，但会抑制某些细胞因子（TNFα，IFNγ和IL-2）和干扰素反应基因（IRF-1和PIM-1）的表达，以及它们的时程Fe2O3-NPs的内吞作用及其对细胞因子和干扰素应答基因表达的影响是相容的。我们得出结论，Fe2O3-NPs可以被Jurkat细胞内吞并在细胞内起作用。 Fe2O3-NPs通过氧化NADPH从而降低Jurkat细胞中Kv1.3通道的电流密度并延缓其失活和恢复动力学，从而破坏Kv beta 2辅助亚基的氧化还原活性，从而导致Kv1的改变。 .3通道功能。这些结果表明，氧化铁纳米粒子可能通过干扰Kv1.3通道的活性来影响T细胞功能。此外，Fe2O3-NPs对某些炎症细胞因子和干扰素应答基因表达的抑制作用表明，氧化铁纳米颗粒可能对T细胞免疫活性和抗炎作用发挥调节作用。

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