The role of endoplasmic reticulum stress in emphysema results from cigarette smoke exposure.

Apoptosis is of considerable importance in the pathogenesis of emphysema, and recent studies show that endoplasmic reticulum (ER) stress is involved in emphysema. In our research, we investigated the role of protein kinase RNA (PKR)-like ER kinase (PERK)/ eukaryotic initiation factor 2 alpha (eIF2α) pathway, the CCAAT enhancer-binding protein-homologous protein (CHOP) expression, caspase-12 activation and apoptosis in emphysema results from cigarette smoke (CS) exposure. Expression of phosphorylated-PERK (p-PERK), phospholated-eIF2α (p-eIF2α),CHOP and caspase-12 as well as the apoptosis rate are remarkably increased in rats after exposure to 2 months CS compared with control rats, significantly elevated in rats exposed to 4 months CS over rats exposed only to 2 months CS, and slightly decreased in ex-smoking rats in contrast to rats exposed to 4 months CS. Taken together, our results show that CS induces ER stress in lung epithelial cells, which may subsequently lead to lung injury in rats, and this might be a novel target for protection of pulmonary epithelial cells from ER stress injury in emphysema.