An increasing body of evidence suggests that apoptosis of structural cells in the lung might be an important upstream event in the pathogenesis of chronic obstructive pulmonary disease (COPD).AP-2α is one of the important transcription factors involved in the modulation of apoptosis in carcinogenesis and idiopathic-dilated cardiomyopathy.The relationship between AP-2α and apoptosis in COPD remains to be elucidated.The aim of the present study was to investigate the expression of AP-2α in the lung tissues of rats with COPD induced by smoking and its possible protective effect on cigarette smoke extract (CSE) induced endothelial cell apoptosis.Sprague-Dawley rats (n=24) were randomly assigned to normal and COPD groups.The COPD group was exposed to smoke from 20 commercial unfiltered cigarettes for 80 d before morphological assessment of the lung tissue was performed.The expression of AP-2α in lung tissues was measured by Western blotting.To demonstrate the relationship between apoptosis and AP-2α,in vitro cell experiments were carried out.Cells were treated with different concentrations of CSE before proliferation was measured by MTT.Apoptosis was then determined by Hoechst staining and the expression of cleaved caspase-3 and AP-2α by Western blotting over time following treatment with 5% CSE.Cells were then infected with an AP-2α adenovirus vector and the expression of cleaved caspase-3 and AP-2α was compared to the control groups by Western blotting.The COPD group showed larger air spaces and significant decrease of FEV 0.3/FVC compared with the rats in the control group (P<0.05).The expression of AP-2α was significantly higher in the lung tissue of rats with COPD compared with those of controls (P<0.05).In the ECV304 cells,CSE induced apoptosis (P<0.01) and caspase-3 activation in a time-dependent manner and reduced the cell proliferation rate in a dose-dependent manner (P<0.005).Moreover,5% CSE treatment increased endogenous AP-2α protein expression.AP-2α overexpression inhibited 5% CSE-induced cell apoptosis and activated caspase-3 expression (P<0.05) AP-2α protects ECV304 cells against CSE-induced apoptosis and may play an important role in smoking induced-apoptosis in COPD. An increasing body of evidence suggests that apoptosis of structural cells in the lung might be an important upstream event in the pathogenesis of chronic obstructive pulmonary disease (COPD) .AP-2α is one of the important transcription factors involved in the modulation of apoptosis in carcinogenesis and idiopathic-dilated cardiomyopathy. The relationship between AP-2α and apoptosis in COPD remains to be elucidated. The aim of the present study was to investigate the expression of AP-2α in the lung tissues of rats with COPD induced by smoking and its possible protective effect on cigarette smoke extract (CSE) induced endothelial cell apoptosis. Sprague-Dawley rats (n = 24) were randomly assigned to normal and COPD groups. The COPD group was exposed to smoke from 20 commercial unfiltered cigarettes for 80 days before morphological assessment of the lung tissue was performed. The expression of AP-2α in lung tissues was measured by Western blotting. To demonstrate the relationship between apopto sis and AP-2α, in vitro cell experiments were carried out. Cells were treated with different concentrations of CSE before proliferation was measured by MTT. Apoptosis was then determined by Hoechst staining and the expression of cleaved caspase-3 and AP-2α by Western blotting over time following treatment with 5% CSE.Cells were then infected with an AP-2α adenovirus vector and the expression of cleaved caspase-3 and AP-2α was compared to the control groups by Western blotting. The COPD group showed larger air spaces and significant decrease of FEV 0.3 / FVC compared with the rats in the control group (P <0.05). The expression of AP-2α was significantly higher in the lung tissue of rats with COPD compared with those of controls (P <0.05). CSE-induced apoptosis (P <0.01) and caspase-3 activation in a time-dependent manner and reduced the cell proliferation rate in a dose-dependent manner (P <0.005) AP-2α protein expression. AP-2 α overexpression inhibited 5% CSE-induced cell apoptosis and activated caspase-3 expression (P <0.05) AP-2α protects ECV304 cells against CSE-induced apoptosis and may play an important role in smoking induced-apoptosis in COPD.