INTRODUCTIONOur lungs have a vital role in mediating the exchange of oxygen and carbon dioxide between the air we breathe and the body.This function is under constant pressure as inhaled air contains numerous particle...INTRODUCTIONOur lungs have a vital role in mediating the exchange of oxygen and carbon dioxide between the air we breathe and the body.This function is under constant pressure as inhaled air contains numerous particles,gasses,and microorganisms that may cause injury and infection to the lungs.Removal and neutralization of potential harmful substances from inhaled air is a main function of the airway epithelium.展开更多
To investigate the effect of lithium on cell cycle progression of airway epithelial cells, primary pig tracheobronchial epithelial cells were incubated with lithium chloride (LiCl) at different concentrations (0, 5 mm...To investigate the effect of lithium on cell cycle progression of airway epithelial cells, primary pig tracheobronchial epithelial cells were incubated with lithium chloride (LiCl) at different concentrations (0, 5 mmol/L, and 10 mmol/L) and time (12 h, 16 h and 24 h). After the treatment, cells were counted, cell cycle profile was measured by BrdU labeling and flow cytometry, and expression of cyclin D1 and cyclin B1 were detected by Western blotting. The results showed that after 24h of 10mmol/L but not 5mmol/L LiCl treatment, proliferation of cells was slowed down as manifested by delayed confluence and cell number accumulation (P<0.05). Lithium did not change the percentage of cells in S phase (P>0.05), but 24 h incubation with 10 mmol/L LiCl induced a G 2/M cell cycle arrest. Furthermore, 10mmol/L LiCl elevated cyclin D1 expression after 12h treatment, while expression of cyclin B1 increased more significantly after 24h incubation. These data demonstrate that lithium inhibits proliferation of pig airway epithelial cells by inhibiting cell cycle progression, and suggest that lithium-sensitive molecule(s) such as glycogen synthase kinase 3 may have a role in the regulation of growth of airway epithelial cells.展开更多
Asthma is a worldwide prevalent disease that is a .considerable health burden in many countries. In recent years, the airway epithelium is increasingly recognized as a central contributor to the pathogenesis of asthma...Asthma is a worldwide prevalent disease that is a .considerable health burden in many countries. In recent years, the airway epithelium is increasingly recognized as a central contributor to the pathogenesis of asthma. One of the most highly induced genes in epithelial ceils in experimental allergic airway disease is the third murine calcium-activated chloride channel homologue （mclca3, alias gob-5）. Its human homology protein is hCLCA, which has been identified as clinically relevant molecules in diseases with secretory dysfunctions including asthma and cystic fibrosis.展开更多
文摘INTRODUCTIONOur lungs have a vital role in mediating the exchange of oxygen and carbon dioxide between the air we breathe and the body.This function is under constant pressure as inhaled air contains numerous particles,gasses,and microorganisms that may cause injury and infection to the lungs.Removal and neutralization of potential harmful substances from inhaled air is a main function of the airway epithelium.
基金ThisprojectwassupportedbyagrantfromNationalNaturalScienceFoundationofChina (No .30 2 0 0 115 )
文摘To investigate the effect of lithium on cell cycle progression of airway epithelial cells, primary pig tracheobronchial epithelial cells were incubated with lithium chloride (LiCl) at different concentrations (0, 5 mmol/L, and 10 mmol/L) and time (12 h, 16 h and 24 h). After the treatment, cells were counted, cell cycle profile was measured by BrdU labeling and flow cytometry, and expression of cyclin D1 and cyclin B1 were detected by Western blotting. The results showed that after 24h of 10mmol/L but not 5mmol/L LiCl treatment, proliferation of cells was slowed down as manifested by delayed confluence and cell number accumulation (P<0.05). Lithium did not change the percentage of cells in S phase (P>0.05), but 24 h incubation with 10 mmol/L LiCl induced a G 2/M cell cycle arrest. Furthermore, 10mmol/L LiCl elevated cyclin D1 expression after 12h treatment, while expression of cyclin B1 increased more significantly after 24h incubation. These data demonstrate that lithium inhibits proliferation of pig airway epithelial cells by inhibiting cell cycle progression, and suggest that lithium-sensitive molecule(s) such as glycogen synthase kinase 3 may have a role in the regulation of growth of airway epithelial cells.
文摘Asthma is a worldwide prevalent disease that is a .considerable health burden in many countries. In recent years, the airway epithelium is increasingly recognized as a central contributor to the pathogenesis of asthma. One of the most highly induced genes in epithelial ceils in experimental allergic airway disease is the third murine calcium-activated chloride channel homologue （mclca3, alias gob-5）. Its human homology protein is hCLCA, which has been identified as clinically relevant molecules in diseases with secretory dysfunctions including asthma and cystic fibrosis.
