Tabagism is the main cause of chronic obstructive pulmonary disease (COPD). Cigarette smoke could induce the synthesis of heat shock proteins 70 (HSP70) wich is suspected to play a protective role against lung injury. The aim of this work was to study the time course of the HSP70 expression at a transcriptomic and proteinic level in a murine model of COPD. Mice groups were exposed for 24 weeks to fresh air or to cigarette smoke (250 TPM). Pulmonary emphysema was measured using morphometric analysis to determine the mean linear intercept (Lm) in mice sacrificed at the following times: 1, 4, 8, 12, 20, 24 weeks. Levels of HSP70 mRNAs and the corresponding proteins were measured by microarrays analysis (1, 4, 8, 12 weeks) and western blots (1, 4, 8, 12, 20, 24 weeks) respectively. Emphysema was yet detected after 12 weeks (Lm of control mice: 56,3  3,62 mm Vs Lm of expose mice: 59,6  3,59 mm) and progressed until the end of the exposure (56,6  2,99 mm Vs 61,9  3,55 mm). A significant 50% HSP70 mRNAs decrease was detected during the three first months exposure while the HSP70 levels remained constant in all groups. In conclusion, the development of emphysema in mice exposed to cigarette smoke is associated with a decrease in the level of HSP70 mRNAs without any change in their protein expression, suggesting a limited protective role in this model.

This work was supported by the Walloon region and the University of Liège Special Research Funds.