Expression of Endoplasmic Reticulum Stress-Associated Protein IRE1 and JNK in Lung Tissues of Smoking Induced COPD Model RatsAuthor(s): Li-Le Wang, Rui-Cheng Hu*, Shuang-Xiang Tan, Ai-Guo Dai, Jian-Lu Su, Ming Xu, Chun-Chu Kong, Yun-Rong Chen, Dai-Yan Fu, Jie Li, Gui-Xiang Gan, Chang-Yu Huang, Bin-Bin Chen and Mo Liang (China)
Aim: To investigate the expression of IRE1 (inositol-requiringenzyme 1) and JNK (c-Jun N-terminal kinase) in lung tissue of cigarette smoke (CS) induced chronic obstructive pulmonary disease (COPD) rats.
Methods: Adult male Wistar rats (n=40) were randomly divided into 4 groups with 10 rats in each group: control group, CS-2 group (exposed to CS for 2 months), CS-4 group (exposed to CS for 4 months) and ex-smoking group (quit smoking for 1 month after exposed to CS for 4 months). The percentage of forced expiratory volume in 0.3 seconds to forced vital capacity (FEV0.3/FVC) and peak expiratory flow (PEF) were measured. TUNEL assay was used to detect apoptotic cells. Immunohistochemistry and Western blotting were used to detect the expression of IRE1, P-IRE1, JNK and P-JNK proteins.
Results: The pulmonary of function greatly decreased in the rats exposed to CS for 2 months in comparison with control group (P<0.05), markedly decreased in the rats exposed to CS for 4 months as compared with the rats after exposure to CS for 2 months (P<0.05) and was improved little in ex-smoking rats (P>0.05). The apoptotic cells were markedly increased in the rats exposed to CS for 2 months and were ever more in the rats exposed to CS for 4 months. The apoptotic cells were alveolar epithelial cell âÂ (ACEâÂ ), ACE âÂ ¡, vascular endothelial cells and bronchial epithelial cells. The protein level of p-IRE1 (phospho-inositol-requiringenzyme 1) and p-JNK (phospho-c-Jun N-terminal kinase) were remarkably increased in the rats after exposure to CS for 2 months compared with the control rats (P<0.05), significantly elevated in the rats exposed to CS for 4 months (P>0.05).
Conclusion: CS promotes the development of COPD by inducing the expression of endoplasmic reticulum stress-associated protein IRE1 and JNK.