Published ahead of print on September 15, 2006, doi:10.1165/rcmb.2006-0259RC Am. J. Respir. Cell Mol. Biol., Volume 36, Number 2, February 2007, 147-151 A more recent version of this article appeared on February 1, 2007
Submitted on July 17, 2006 Modulation of Glutaredoxin-1 Expression in a Mouse Model of Allergic Airway DiseaseNiki L Reynaert1,1 Department of Respiratory Medicine, Nutrition and Toxicology Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands; Department of Pathology, University of Vermont, Burlington, VT, USA, 2 Department of Respiratory Medicine, Nutrition and Toxicology Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands * To whom correspondence should be addressed. E-mail: yjanssen{at}uvm.edu.
Glutaredoxins (GRX) are antioxidant enzymes that preferentially catalyze the reduction of protein-glutathione mixed disulfides. The formation of mixed disulfides with GSH is known as S-glutathionylation, a posttranslational modification that is emerging as an important mode of redox signaling. Since asthma is a disease that is associated with increased oxidative stress and altered antioxidant defenses, we investigated the expression of GRX in a murine model of allergic airway disease. Sensitization and challenge of C57BL/6 mice with ovalbumin resulted in increased expression of GRX1 mRNA, as well as increased amounts of GRX1 protein and total GRX activity in the lung. Because GRX-1 expression is prominent in bronchial epithelium, we isolated primary epithelial cells from mouse trachea to investigate the presence of GRX. Primary tracheal epithelial cells were found to express both GRX1 and 2 mRNA and detectable GRX activity. Treatment with IFN
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