Zinc oxide particles induce inflammatory responses in vascular endothelial cells via NF-κB signaling
Autor: | Tsui-Chun Tsou, Feng-Yuan Tsai, How-Ran Chao, Tsun-Jen Cheng, Lin-Ai Tai, Ho-Jane Lin, Szu-Ching Yeh |
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Rok vydání: | 2010 |
Předmět: |
Environmental Engineering
Endothelium Health Toxicology and Mutagenesis medicine.medical_treatment Inflammation Umbilical vein chemistry.chemical_compound medicine Humans Environmental Chemistry Waste Management and Disposal Cells Cultured Cell Proliferation Cell Death Dose-Response Relationship Drug Chemistry Cell growth Cell adhesion molecule NF-kappa B Endothelial Cells NF-κB Intercellular Adhesion Molecule-1 Glutathione Pollution Cell biology IκBα Cytokine medicine.anatomical_structure Immunology Nanoparticles Zinc Oxide medicine.symptom Signal Transduction |
Zdroj: | Journal of Hazardous Materials. 183:182-188 |
ISSN: | 0304-3894 |
DOI: | 10.1016/j.jhazmat.2010.07.010 |
Popis: | This study investigated inflammatory effects of zinc oxide (ZnO) particles on vascular endothelial cells. The effects of 50 and 100-nm ZnO particles on human umbilical vein endothelial cells (HUVECs) were characterized by assaying cytotoxicity, cell proliferation, and glutathione levels. A marked drop in survival rate was observed when ZnO concentration was increased to 45 μg/ml. ZnO concentrations of ≤3 μg/ml resulted in increased cell proliferation, while those of ≤45 μg/ml caused dose-dependent increases in oxidized glutathione levels. Treatments with ZnO concentrations ≤45 μg/ml were performed to determine the expression of intercellular adhesion molecule-1 (ICAM-1) protein, an indicator of vascular endothelium inflammation, revealing that ZnO particles induced a dose-dependent increase in ICAM-1 expression and marked increases in NF-κB reporter activity. Overexpression of IκBα completely inhibited ZnO-induced ICAM-1 expression, suggesting NF-κB plays a pivotal role in regulation of ZnO-induced inflammation in HUVECs. Additionally, TNF-α, a typical inflammatory cytokine, induced ICAM-1 expression in an NF-κB-dependent manner, and ZnO synergistically enhanced TNF-α-induced ICAM-1 expression. Both 50 and 100-nm ZnO particles agglomerated to similar size distributions. This study reveals an important role for ZnO in modulating inflammatory responses of vascular endothelial cells via NF-κB signaling, which could have important implications for treatments of vascular disease. |
Databáze: | OpenAIRE |
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