Effects of exposure to cigarette smoke on expression of Wnt3a and β-catenin protein in rat lung tissue

Abstract

Objective To investigate the effects of cigarette smoke(CS) exposure on expression of Wnt3a and β-catenin protein in rat lung tissue.Methods Twenty female SD rats were allocated to 2 groups (n=10 each) by random digit table:the control group and CS exposure group(model group).Rats in model group were subjected to twice-daily 45-min CS exposure,while the rats in control group were kept isolated from CS.The animals were sacrificed on day 100 to be harvested for lung tissues which were then studied for pathological morphology under light microscopy,expressions of α-smooth muscle actin (α-SMA),Wnt3a and β-catenin proteins by immunohistochemistry, and thickness of bronchial smooth muscle layer by morphometry.Results The rats in model group showed chronic inflammation,emphysema-like change and thickening of small airway walls and smooth muscle layers in the lung tissues.In both groups,α-SMA protein was localized in the smooth muscle layer of airway and vessel.The mean thickness of bronchial smooth muscle was significantly greater in the model group than those in control group [ (3.06±0.62) μm vs ( 1.86±0.43) μm,P＜0.05].Wnt3a and β-catenin were mainly expressed in the bronchial and alveolar epithelium.In model group and control group,the levels of Wnt3a expression were 74.54 ±4.14 vs 89.24 ± 3.02 in bronchial epithelial cells,and 91.97 ± 2.50 vs 110.46 ± 3.85 in alveolar epithelial cells,with significant differences between groups (both P＜0.05) ; the levels of β-catenin expression were 86.97±4.87 vs 103.18±3.77 in cytoplasm of bronchial epithelial cells,and 95.75 ±3.91 vs 116.12±5.76 in nuclei of bronchial epithelial cells,106.24±4.57 vs 128.81±3.96 in cytoplasm of alveolar epithelial cells,and 125.44±4.89 vs 152.90±4.10 in nuclei of alveolar epithelial cells,with significant differences between groups (all P＜0.05).Conclusions Cigarette smoke may induce up-regulation of Wnt3a and β-catenin proteins in rat lung tissue. Key words: Pulmonary disease,chronic obstructive; Wnt proteins; Wnt-β-catenin signaling pathway; Airway remodeling; Cigarette smoke; Rats