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B AND POST-TRANSLATIONAL MODIFICATIONS OF HISTONE DEACETYLASE IN IN MACROPHAGES
1 Department of Environmental Medicine, University of Rochester Medical Center, Rochester, NY, USA
2 Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY, USA
3 Pfizer Global Research and Development,, Sandwich, England, United Kingdom
* To whom correspondence should be addressed. E-mail: rfan_Rahman{at}urmc.rochester.edu.
Cigarette smoke-mediated oxidative stress induces an inflammatory response in the lungs by stimulating the release of proinflammatory cytokines. Chromatin remodeling due to histone acetylation and deacetylation is known to play an important role in transcriptional regulation of proinflammatory genes. The aim of this study was to investigate the molecular mechanism(s) of inflammatory responses caused by cigarette smoke extract (CSE) in the human macrophage-like cell line (MonoMac6) and whether the treatment of these cells with the antioxidant glutathione (GSH) monoethyl ester, or modulation of the thioredoxin redox system, can attenuate cigarette smoke-mediated interleukin (IL)-8 release. Exposure of MonoMac6 cells to CSE (1% and 2.5%) increased IL-8 and TNF-
production versus control at 24 hours and was associated with significant depletion of GSH levels associated with increased ROS release in addition to activation of NF-
B. Inhibition of IB kinase ablated the CSE-mediated IL-8 release, suggesting this process is dependent upon the NF-k pathway. CSE also reduced histone deacetylase (HDAC) activity and HDAC1, HDAC2 and HDAC3 protein levels. This was associated with post-translational modification of HDAC1, 2 and 3 protein by nitrotyrosine and aldehyde-adduct formation. Pretreatment of cells with GSH monoethyl ester, but not thioredoxin/thioredoxin reductase, reversed cigarette smoke-induced reduction in HDAC levels and significantly inhibited IL-8 release. Thus cigarette smoke-induced release of IL-8 is associated with activation of NF-B via IB kinase and reduction in HDAC levels/activity in macrophages. Moreover, cigarette smoke-mediated pro-inflammatory events are regulated by the redox status of the cells.
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