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Title: Amorphous silica particles promote inflammatory gene expression through the redox sensitive transcription factor, AP-1, in alveolar epithelial cells.

Authors: Singal, Madhuri; Finkelstein, Jacob N

Published In Exp Lung Res, (2005 Jul-Aug)

Abstract: Ultrafine particulate (UFP) matter, from environmental or industrial exposure, can induce expression of inflammatory mediators and promote production of reactive oxygen species. Previous studies showed various cellular stresses activate signaling pathways operating through specific transcription factors (TFs), activator protein (AP)-1 and nuclear factor (NF)-kappaB, known to regulate inflammatory gene expression. Exposing MLE15 cells to inflammatory, or UFP, stimuli increased macrophage inflammatory protein (MIP)-2 protein, in the absence of the NF = kappaB inhibitor IkappaBc degradation, synergistically increasing in the presence of proteosomal inhibition. Although thiol antioxidants attenuate MIP-2 induction, mitogen-activated protein kinase (MAPK) inhibitors significantly inhibit MIP-2 protein production. This suggests UFP promote inflammatory gene expression through the redox responsive TF AP-1.

PubMed ID: 16019989 Exiting the NIEHS site

MeSH Terms: Animals; Antioxidants/pharmacology; Butylated Hydroxyanisole/pharmacology; Cell Line; Chemokine CXCL2; Chemokines/genetics; Enzyme Inhibitors/pharmacology; Epithelial Cells/drug effects; Epithelial Cells/immunology*; Epithelial Cells/metabolism; Gene Expression Regulation/drug effects; Gene Expression Regulation/immunology; Heme Oxygenase (Decyclizing)/metabolism; Heme Oxygenase-1; I-kappa B Proteins/metabolism; MAP Kinase Signaling System/drug effects; Muridae; NF-KappaB Inhibitor alpha; Oxidation-Reduction; Pneumonia/chemically induced; Pneumonia/immunology; Pneumonia/physiopathology*; Pulmonary Alveoli/cytology; Pulmonary Alveoli/immunology*; Pulmonary Alveoli/metabolism; Respiratory Mucosa/cytology; Respiratory Mucosa/immunology; Respiratory Mucosa/metabolism; Silicon Dioxide/pharmacology*; Transcription Factor AP-1/metabolism*

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