Source: Annual Congress 2001 - Inflammatory mechanisms of COPD
Disease area: Airway diseases

Abstract

Histone deacetylase (HDAC) is associated with gene silencing or transcriptional repression. We have demonstrated that smoking and oxidative stress decreased HDAC activity in lung tissue, alveolar macrophage or culture epithelial cell, and there is good correlation between HDAC activity and proinflammatory cytokine production in alveolar macrophage. Smoking, an oxidative stress, is the major cause of chronic obstructive pulmonary disease (COPD). We investigated HDAC activity and gene expression in COPD. Lung tissue was taken from smokers and non-smokers with lung cancer and from COPD patients operated surgically. Total HDAC activity of COPD (352.9±]120.4 dpm, n=5) is similar to that of smokers (267.7±]80.70 dpm, n=6) and much lower than those of non-smokers (3008±]1140 dpm, n=7). HDAC2 and 5 mRNA levels were decreased in COPD compared to those of smokers and normals, however, HDAC1, 4, 6 mRNA levels did not change. The protein level of HDAC 2, 3, 5 in COPD was decreased and those of HDAC 1 and 4 did not change. HDAC 2 immunoprecipitated from COPD lung was nitrosylated suggesting decreased activity as we have demonstrated previously (abstract ERS 2000). These results suggest reduced HDAC activity is involved in the development of COPD.
This abstract is funded by Sankyo and CRC (Brompto Hospital).

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Citations should be made in the following way:
K. Ito, S. I. Watanabe, S. Kharitonov, T. Hanazawa, I. M. Adcock, P. J. Barnes (London, United Kingdom). Histone deacetylase activity and gene expression in COPD patients. Eur Respir J 2001; 16: Suppl. 31, 2115

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