Transcriptomics-based characterization of smoking and cessation effects in mouse lung

COPD is a disorder characterized by the progressive development of airflow limitation that is not fully reversible. Cigarette smoke has been generally accepted as the most important of many risk factors for the development of COPD. We used microarray technology to perform comprehensive gene expression profiling of smoke exposure and cessation effects in mouse lung tissue. Mice received nose-only exposure of 4% mainstream cigarette smoke or air (sham exposure) for 2 hours/day, 5 days/week for 2, 12 or 24 weeks. Mice undergoing smoke cessation received cigarette smoke exposure for 12 weeks, and then sham exposure for 12 weeks.