Ultrafine particles from diesel engines induce vascular oxidative stress via JNK activation
| Autor: | Constantinos Sioutas, Tyler Beebe, Tzung K. Hsiai, Bhavraj Khalsa, Jeffery Cui, Rohit Majumdar, Wakako Takabe, Rongsong Li, Zhi Ning, Lisong Ai |
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| Rok vydání: | 2009 |
| Předmět: |
Antioxidant
medicine.medical_treatment medicine.disease_cause Biochemistry Article Thromboplastin Acetylcysteine chemistry.chemical_compound Tissue factor Superoxides Physiology (medical) medicine Humans Mitogen-Activated Protein Kinase 9 Gene silencing Mitogen-Activated Protein Kinase 8 RNA Small Interfering Aorta Cells Cultured Anthracenes Superoxide Endothelial Cells Cell biology Enzyme Activation Oxidative Stress Gene Expression Regulation chemistry Knockout mouse Nanoparticles Particulate Matter Gasoline Heme Oxygenase-1 Oxidative stress Intracellular medicine.drug |
| Zdroj: | Free Radical Biology and Medicine. 46:775-782 |
| ISSN: | 0891-5849 |
| Popis: | Exposure of particulate air pollution is linked to increased incidences of cardiovascular diseases. Ambient ultra fine particles (UFP) from diesel vehicle engines have been shown to be pro-atherogenic in apoE knockout mice and may constitute a major cardiovascular risk in humans. We posited that circulating nano-sized particles from traffic pollution sources induced vascular oxidative stress via JNK activation in endothelial cells. Diesel UFP were collected from a 1998 Kenworth truck. Intra-cellular superoxide assay revealed that these UFP dose-dependently induced superoxide (O2·-) production in human aortic endothelial cells (HAEC). Flow cytometry (FACS) showed that UFP increased MitoSOX Red intensity specific for mitochondrial superoxide. Protein carbonyl content is increased by UFP as an indication of vascular oxidative stress. UFP also up-regulated hemeoxygenase-1 (HO-1) and tissue factor (TF) mRNA expression, and pre-treatment with antioxidant, N-acetyl cysteine (NAC), significantly decreased their expression. Furthermore, UFP transiently activated JNK in HAEC. Treatment with JNK inhibitor SP600125 and silencing of both JNK1 and JNK2 with siRNA inhibited UFP stimulated O2·- production and mRNA expression of HO-1 and TF. Our findings suggest that JNK activation play an important role in UFP-induced oxidative stress and stress response gene expression. |
| Databáze: | OpenAIRE |
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