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首页> 外文期刊>Cellular immunology >Vascular oxidative stress increases dendritic cell adhesion and transmigration induced by homocysteine.
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Vascular oxidative stress increases dendritic cell adhesion and transmigration induced by homocysteine.

机译:血管氧化应激会增加高半胱氨酸诱导的树突状细胞粘附和转运。

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摘要

Atherosclerosis is a long-term chronic inflammatory and immunological disease. Endothelial dysfunction and the dendritic cell (DC) immune response are pivotal early events in atherogenesis. This study investigated the effects and possible mechanisms of action of homocysteine (Hcy) on DC adhesion to and transmigration between endothelial cells (ECs), and indicated a novel immunoregulatory mechanism by which Hcy induces atherogenesis. When ECs were stimulated with increasing concentrations of Hcy, immunofluorescence showed that endothelial reactive oxygen species (ROS) generation strikingly increased, while nitrite assay showed that nitric oxide (NO) release markedly decreased. Furthermore, DC adhesion and transmigration were significantly increased when ECs were activated by Hcy. However, pretreatment of ECs with antioxidant before Hcy markedly attenuated the induction of DC adhesion and transmigration, dependent on the intracellular ROS decrease and endothelial NO increase. In conclusion, DC adhesion and transmigration are significantly increased by vascular oxidative stress under conditions of elevated Hcy levels. These findings provide insight into the inflammatory processes and immune responses occurring in atherosclerosis induced by Hcy.
机译:动脉粥样硬化是一种长期的慢性炎性和免疫性疾病。内皮功能障碍和树突状细胞(DC)免疫反应是动脉粥样硬化发生中的关键早期事件。这项研究调查了高半胱氨酸(Hcy)对DC粘附至内皮细胞(EC)和在内皮细胞(EC)之间迁移的作用及其可能的作用机制,并指出了Hcy诱导动脉粥样硬化形成的新型免疫调节机制。当EC浓度增加的Hcy刺激时,免疫荧光显示内皮活性氧(ROS)的生成显着增加,而亚硝酸盐测定显示一氧化氮(NO)的释放明显减少。此外,当EC被Hcy激活时,DC粘附和转运明显增加。然而,在Hcy之前用抗氧化剂对EC进行预处理可显着减弱DC粘附和迁移的诱导,这取决于细胞内ROS的减少和内皮NO的增加。总之,在Hcy水平升高的情况下,血管氧化应激会显着增加DC的粘附和迁移。这些发现提供了对由Hcy诱导的动脉粥样硬化中发生的炎性过程和免疫应答的见解。

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