Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5862741 | Toxicology in Vitro | 2011 | 10 Pages |
Abstract
⺠Diesel exhaust particulate (DEP) has been suggested to traverse alveolar barriers. ⺠But, DEP vascular effects may be related to the release of inflammatory cytokines. ⺠We found that direct DEP exposure to endothelium perturbed cell function. ⺠Endothelial responses were greater when co-cultured with DEP exposed macrophages. ⺠DEP vascular effects are likely due to release of soluble factors by macrophages.
Keywords
PM2.5iNOSDEPRT-PCRGSHMCP1AREsBH4tetrahydrobiopterinIL6GCLCFBSGCLMeNOSECE1TNFαPBSGCLGMCSF3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromideDMSOIL1βMTTONOO−ROSinflammationendothelinendothelin-1interleukin 1βinterleukin 6analysis of varianceANOVAtumor necrosis factor αstandard error of the meanDimethylsulfoxideDiesel exhaust particulateparticulate matterfetal bovine seruminducible nitric oxide synthaseendothelial nitric oxide synthaseGranulocyte macrophage colony stimulating factorantioxidant response elementsPhosphate buffered salineglutamate cysteine ligaseSEMNoxsNitric oxidenitric oxide synthasemonocyte chemoattractant protein 1Peroxynitriteglutamate cysteine ligase modifier subunitGlutamate cysteine ligase catalytic subunitGlutathioneReactive oxygen species
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Authors
Chad S. Weldy, Hui-Wen Wilkerson, Timothy V. Larson, James A. Stewart, Terrance J. Kavanagh,