Department of Biological Engineering, Utah State University, Logan, Utah, United States of America.
PLoS One. 2012;7(5):e36885. doi: 10.1371/journal.pone.0036885. Epub 2012 May 25.
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.
暴露于柴油机排气颗粒物（DEPs）是交通相关空气污染的主要来源，由于其对心血管和呼吸系统疾病等人类健康的不良影响，已成为严重的健康关注点。为了阐明暴露于 DEPs 的内皮细胞的生物物理特性（细胞形貌、细胞骨架组织和细胞力学）与功能之间的关系，原子力显微镜（AFM）被应用于分析 DEPs 对人主动脉内皮细胞（HAECs）模型细胞系的毒性作用。荧光显微镜和流式细胞术也被应用于进一步探索 DEP 诱导的 HAECs 细胞毒性。结果表明，DEPs 能够以剂量和时间依赖的方式负性地损害细胞活力并改变细胞膜的纳米结构和细胞骨架成分；分析表明，DEP 诱导的 HAECs 超极化呈现时间依赖性，这意味着 DEP 处理会导致血管舒张，这可以通过细胞生物物理特性（例如细胞弹性）的下调得到支持。这些发现与 DEP 暴露引发重要的生化和生物物理变化，从而对心血管疾病的病理发展产生负面影响的结论一致。例如，DEP 的干预可能是血管舒张的一个原因，这将扩展对与 HAECs 中 DEP 细胞毒性相关的生物物理方面的理解。
