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汞通过细胞膜硫酸脂介导导致红细胞与层粘连蛋白异常黏附。

Mercury leads to abnormal red blood cell adhesion to laminin mediated by membrane sulfatides.

机构信息

Science Faculty, Department of Molecular Biology and Genetics Department, Cumhuriyet University, Sivas, Turkey; Case Biomanufacturing and Microfabrication Laboratory, Mechanical and Aerospace Engineering Department, Case Western Reserve University, Cleveland, OH, USA.

Case Biomanufacturing and Microfabrication Laboratory, Mechanical and Aerospace Engineering Department, Case Western Reserve University, Cleveland, OH, USA.

出版信息

Biochim Biophys Acta Biomembr. 2019 Jun 1;1861(6):1162-1171. doi: 10.1016/j.bbamem.2019.03.008. Epub 2019 Mar 16.

Abstract

Exposure to mercury is associated with numerous health problems, affecting different parts of the human body, including the nervous and cardiovascular systems in adults and children; however, the underlying mechanisms are yet to be fully elucidated. We investigated the role of membrane sulfatide on mercuric ion (Hg) mediated red blood cell (RBC) adhesion to a sub-endothelial matrix protein, laminin, using a microfluidic system that mimics microphysiological flow conditions. We exposed whole blood to mercury (HgCl), at a range of concentrations to mimic acute (high dose) and chronic (low dose) exposure, and examined RBC adhesion to immobilized laminin in microchannels at physiological flow conditions. Exposure of RBCs to both acute and chronic levels of Hg resulted in elevated adhesive interactions between RBCs and laminin depending on the concentration of HgCl and exposure duration. BCAM-Lu chimer significantly inhibited the adhesion of RBCs that had been treated with 50 μM of HgCl solution for 1 h at 37 °C, while it did not prevent the adhesion of 3 h and 24 h Hg-treated RBCs. Sulfatide significantly inhibited the adhesion of RBC that had been treated with 50 μM of HgCl solution for 1 h at 37 °C and 0.5 μM of HgCl solution for 24 h at room temperature (RT). We demonstrated that RBC BCAM-Lu and RBC sulfatides bind to immobilized laminin, following exposure of RBCs to mercuric ions. The results of this study are significant considering the potential associations between sulfatides, red blood cells, mercury exposure, and cardiovascular diseases.

摘要

汞暴露与许多健康问题有关,影响人体的不同部位,包括成人和儿童的神经系统和心血管系统;然而,其潜在机制尚未完全阐明。我们使用一种模拟微生理流动条件的微流控系统,研究了膜神经节苷脂在汞离子(Hg)介导的红细胞(RBC)黏附到内皮基质蛋白层粘连蛋白中的作用。我们将全血暴露于汞(HgCl)中,浓度范围模拟急性(高剂量)和慢性(低剂量)暴露,并在生理流动条件下检查 RBC 黏附到固定化层粘连蛋白的情况。RBC 暴露于急性和慢性水平的 Hg 都会导致 RBC 与层粘连蛋白之间的黏附相互作用增强,这取决于 HgCl 的浓度和暴露持续时间。BCAM-Lu 嵌合体显著抑制了用 50µM 的 HgCl 溶液处理 1 小时的 RBC 的黏附,而不防止 3 小时和 24 小时 Hg 处理的 RBC 的黏附。神经节苷脂显著抑制了用 50µM 的 HgCl 溶液处理 1 小时的 RBC 的黏附,以及用 0.5µM 的 HgCl 溶液处理 24 小时的 RBC 的黏附。我们证明,在 RBC 暴露于汞离子后,RBC 的 BCAM-Lu 和 RBC 神经节苷脂与固定化的层粘连蛋白结合。考虑到神经节苷脂、红细胞、汞暴露和心血管疾病之间的潜在关联,这项研究的结果是有意义的。

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本文引用的文献

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Int J Environ Res Public Health. 2017 Jan 12;14(1):74. doi: 10.3390/ijerph14010074.
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Binding Affinity of Inorganic Mercury and Cadmium to Biomimetic Erythrocyte Membranes.无机汞和镉与仿生红细胞膜的结合亲和力
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