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Dynamic changes of adenomatous polyposis coli protein and glycogen synthase kinase 3#beta# in the repair of the injured airway epithelial cells in smoking mice

Liu Mingge, Li Naping, Wu Renliang, Ma Yan, Hong Yuanzhi, Tian Dan, Zhu Min

Department of Pathology,Tongji Medical College,Huazhong University of Science and Technology,Pulmonary Disease Laboratory,the Ministry of Health of China.Wuhan 430030,Hubei

Abstract

To investigate the roles of adenomatous polyposis coli (APC) protein and glycogen synthase kinase3#beta# (GSK3#beta#) of smoking murine model in the repair of the injured airway epithelial cells (AECs) in different stages, 30 male Kun-Ming mice were randomly divided into two groups, the control group and the smoking group. There were 24 mice in smoking group, 6 animals were separately killed at the end of the 1st, 4th, 8th and 12th week after smoking. Then the following tests were undertaken: (1) HE staining of lung section to observe the morphological changes of the bronchi in the smoking mice. (2) Immunohistochemical staining of APC protein and GSK3#beta# in the AEC. (3) Western blotting was used to detect the levels of APC protein, GSK3#beta# and phosphoric GSK3#beta# (p-GSK3#beta#) in pulmonary tissue. (4) Observing the localizations of APC protein and GSK3#beta# in the AEC by immunofluorescence technique. The results showed: (1) Airway epithelial cells showed predominant injury (1-, 4-week), repair (8-week) and reinjury (12-week). The experimental results indicated that the model of smoking mice was duplicated successfully. (2) Immunohistochemical results showed that the expression of APC protein in the AEC increased after 1-week smoking (0.458±0.062 vs 0.399±0.060, P<0.05 vs control), but was significantly decreased at the end of 4th week (0.339±0.056, P<0.01 vs control) and increased at the end of the 8th and 12th week (0.387±0.041, 0.378±0.037, P<0.05 vs 4-week). The expressions of GSK3#beta# in the AEC of smoking mice obviously decreased (P<0.01 or P<0.05 vs control). (3) Western blotting showed that the expressions of APC protein and GSK3#beta# in lung tissue were consistent with the results of immunohistochemistry; the levels of P-GSK3#beta# in all smoking model were higher than that in control. (4) The results of immunofluorescence showed that APC protein was localized mainly near the regions of epithelial cell membrane at the end of 1st and 8th week after smoking, which are dissimilar with the localization in control, and this change was not seen in the locations of GSK3#beta#. Taken together, these results demonstrate that the expressions and localizations of APC protein, GSK3#beta# and the activity of GSK3#beta# are dynamically changed in the AEC with experimental smoking injury at different phases, suggesting that APC protein and GSK3#beta# may be involved in the regulation of migration and proliferation of airway epithelial cell, and play an important role in the process of repair of airway epithelium injury.

Key words: adenomatous polyposis coli protein;glycogen synthase kinase 3#beta#;smoking;airway epithelial cells;repair

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Citing This Article：

Liu Mingge, Li Naping, Wu Renliang, Ma Yan, Hong Yuanzhi, Tian Dan, Zhu Min. Dynamic changes of adenomatous polyposis coli protein and glycogen synthase kinase 3#beta# in the repair of the injured airway epithelial cells in smoking mice. Acta Physiol Sin 2006; 58 (3): (in Chinese with English abstract).