Heat shock protein 27 and cyclophilin A associate with the pathogenesis of COPD.

Background And Objective: COPD is a global disease characterized by chronic bronchitis and obstructive emphysema. Its pathogenesis is not fully understood. This study aimed to use proteomics to provide new insights into the mechanisms of COPD.

Methods: Protein lysates were prepared from lung tissue samples harvested from never-smokers, non-COPD smokers and COPD smokers, and were analysed using 2-dimensional gel electrophoresis. Differentially expressed proteins were identified using mass spectrometry. The differential expression of heat shock protein 27 (Hsp27) and cyclophilin A (CyPA) was validated by immunohistochemistry and western blotting.

Results: Twenty-four proteins were identified by mass spectrometry as being differentially expressed among the three groups of subjects. The main functions of these proteins involve basic metabolism, oxidation/reduction, coagulation/fibrinolysis, protein degradation, signal transduction, inflammation and cell growth/differentiation/apoptosis. Proteomic analysis revealed that the expression of Hsp27 and CyPA was upregulated in smokers, and this upregulation was particularly marked in COPD smokers. The variation in expression of Hsp27 and CyPA between the groups was confirmed by immunohistochemistry and western blotting.

Conclusions: Hsp27 and CyPA are associated with the pathogenesis of COPD, and smoking contributes to the overexpression of these proteins.