Toxicity effects of short term diesel exhaust particles exposure to human small airway epithelial cells (SAECs) and human lung carcinoma epithelial cells (A549).
Toxicity effects of short term diesel exhaust particles exposure to human small airway epithelial cells (SAECs) and human lung carcinoma epithelial cells (A549).
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DOI：
10.1016/j.toxlet.2012.10.016
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发表时间：
2012-12-17
影响因子：
3.5
通讯作者：
Zhou A
中科院分区：
文献类型：
--
作者：
Tang M;Li Q;Xiao L;Li Y;Jensen JL;Liou TG;Zhou A
在本研究中，应用共焦拉曼光谱、原子力显微镜（AFM）和多重ELISA来分析正常人原代小气道上皮细胞（SAEC）和人肺癌上皮A549细胞对体外短期DEP暴露（长达2小时）的生物物理反应（生物力学和生物光谱）。拉曼光谱揭示了与未暴露的对照细胞相比，DEP 诱导的细胞中特定的细胞生物分子变化。主成分分析成功地应用于分析多个单个细胞的对照组和处理组之间的光谱差异，并表明细胞核比其他细胞位置更敏感。 AFM 测量表明，DEP 暴露 2 小时会导致细胞弹性显着降低，膜表面粘附力发生显着变化。通过多重 ELISA 测量的细胞因子和趋化因子的产生证明了两种细胞类型中 DEP 诱导的炎症反应。
In this study, confocal Raman spectroscopy, atomic force microscope (AFM) and multiplex ELISA were applied to analyze the biophysical responses (biomechanics and biospectroscopy) of normal human primary small airway epithelial cells (SAECs) and human lung carcinoma epithelial A549 cells to in vitro short term DEP exposure (up to 2 h). Raman spectra revealed the specific cellular biomolecular changes in cells induced by DEP compared to unexposed control cells. Principal component analysis was successfully applied to analyze spectral differences between control and treated groups from multiple individual cells, and indicated that cell nuclei are more sensitive than other cell locations. AFM measurements indicated that 2 h of DEP exposure induced a significant decrease in cell elasticity and a dramatic change in membrane surface adhesion force. Cytokine and chemokine production measured by multiplex ELISA demonstrated DEP-induced inflammatory responses in both cell types.
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影响因子：
3.5
作者：
Cross SE;Jin YS;Lu QY;Rao J;Gimzewski JK
通讯作者：
Gimzewski JK
影响因子：
3.5
作者：
Cross, Sarah E.;Jin, Yu-Sheng;Gimzewski, James K.
通讯作者：
Gimzewski, James K.
影响因子：
3.4
作者：
Chan, JW;Taylor, DS;Huser, T
通讯作者：
Huser, T
影响因子：
158.5
作者：
HOGG, JC;MACKLEM, PT;THURLBECK, WM
通讯作者：
THURLBECK, WM
影响因子：
14.2
作者：
DiazSanchez, D;Tsien, A;Saxon, A
通讯作者：
Saxon, A