engleski

Cigarette smoke induces differential activation of MAP kinase signaling pathways in alveolar epithelial cells

Chronic obstructive pulmonary disease (COPD) is a global health problem characterized by chronic inflammation leading to progressive airflow limitation that is a result of an abnormal response to inhaled particles and gases in the lung. Development of oxidative stress is second important element in the pathogenesis of COPD. The presence of oxidative stress in the airways of smokers, the largest population of COPD patients, is a consequence of direct inhalation of cigarette smoke. Cells respond to various intracellular and extracellular stimuli by generating specific responses mediated by a complex network of signalling pathways. The mitogen-activated protein (MAP) kinase signalling cascade mediates a variety of biological events, including proliferation, inflammation and apoptosis, and can be activated by different stimuli. In this study, we examined the expression and activation of MAP kinases (ERK, p38, JNK) in A549 alveolar epithelial cell line upon the exposure to cigarette smoke extract (CSE). A549 alveolar epithelial cells were exposed to various concentrations of CSE (0 %, 1.25 %, 2.5 %, 5 %, 10 % and 20 %) for both 4 and 24 hours. Expression and activation of MAP kinases (ERK, p38, JNK) were detected by Western blotting. Exposure of alveolar epithelial cells to CSE did not affect the expression of MAP kinases (ERK, p38, JNK). However, differential activation of MAP kinases was observed. CSE induced the activation of ERK and p38 in a dose-dependent manner, while JNK activation was not observed. Our results have shown that cigarette smoke impacts the MAP kinase signaling pathways. Activation of p38 could be related to inflammatory response and apoptosis observed in lungs of COPD patients.

COPD ; cigarette smoke ; MAP kinases ; ERK ; p38 ; JNK ; inflammation ; apoptosis

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