Biophysical assessment of single cell cytotoxicity: diesel exhaust particle-treated human aortic endothelial cells.

Biophysical assessment of single cell cytotoxicity: diesel exhaust particle-treated human aortic endothelial cells.
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DOI:
10.1371/journal.pone.0036885
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Nguyen KT
Nguyen KT
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Wu Y;Yu T;Gilbertson TA;Zhou A;Xu H;Nguyen KT

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柴油机尾气颗粒物(DEPs)是交通相关空气污染的主要来源之一,对人体健康有严重影响,包括心血管疾病和呼吸系统疾病。为了阐明DEPs对内皮细胞的生物物理特性(细胞形态、细胞骨架结构和细胞力学)与功能的关系,应用原子力显微镜(AFM)研究了DEPs对人主动脉内皮细胞(HAECs)的毒性作用。荧光显微镜和流式细胞术也被用来进一步探讨DEP诱导的HAECs的细胞毒性。结果显示,DEP可以以剂量和时间依赖性方式负面地损害细胞活力并改变膜纳米结构和细胞骨架组分;并且分析表明,DEP诱导的HAEC超极化以时间依赖性方式出现,这意味着DEP处理将导致血管舒张,这可以通过下调细胞生物物理特性(例如,细胞弹性)。这些发现与DEP暴露引发重要的生物化学和生物物理变化的结论一致,这些变化将对心血管疾病的病理发展产生负面影响。例如,DEP干预将是血管舒张的一个原因,这将扩大对与HAEC中DEP细胞毒性相关的生物物理方面的理解。
Exposure to diesel exhaust particles (DEPs), a major source of traffic-related air pollution, has become a serious health concern due to its adverse influences on human health including cardiovascular and respiratory disorders. To elucidate the relationship between biophysical properties (cell topography, cytoskeleton organizations, and cell mechanics) and functions of endothelial cells exposed to DEPs, atomic force microscope (AFM) was applied to analyze the toxic effects of DEPs on a model cell line from human aortic endothelial cells (HAECs). Fluorescence microscopy and flow cytometry were also applied to further explore DEP-induced cytotoxicity in HAECs. Results revealed that DEPs could negatively impair cell viability and alter membrane nanostructures and cytoskeleton components in a dosage- and a time-dependent manner; and analyses suggested that DEPs-induced hyperpolarization in HAECs appeared in a time-dependent manner, implying DEP treatment would lead to vasodilation, which could be supported by down-regulation of cell biophysical properties (e.g., cell elasticity). These findings are consistent with the conclusion that DEP exposure triggers important biochemical and biophysical changes that would negatively impact the pathological development of cardiovascular diseases. For example, DEP intervention would be one cause of vasodilation, which will expand understanding of biophysical aspects associated with DEP cytotoxicity in HAECs.
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