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Aquaporin-3 Protects Airway Epithelial Cells in COPD by Regulating Stearoyl-Coadesaturase-1
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A3813 - Aquaporin-3 Protects Airway Epithelial Cells in COPD by Regulating Stearoyl-Coadesaturase-1
Author Block: J. Zhou, G. Zhang, M. Chang, Y. Song, Q. Hong, C. Bai; Department of Pulmonary Medicine, Fudan University, Shanghai, China.
Introduction: Airway epithelial cells are massively damaged in patients with chronic obstructive pulmonary disease (COPD). Aquaporin-3 (AQP3) is highly expressed in the airway epithelial cells in lung. In this study, we investigated the role of AQP3 in COPD airway epithelial cells. Method: The wild-type and AQP3-knockout (AQP3-/-) mice were treated with cigarette smoke and lipopolysaccharides to establish a mouse model of COPD. Human bronchial epithelial cells (HBECs) were stimulated with cigarette smoke extract. Alveolar structure and inflammatory cell infiltration were examined by hematoxylin and eosin staining. The levels of IL-6 and TNF-a in serum and alveolar lavage fluid were evaluated by ELISA. The expression of AQP3 in the lung tissue were detected by immunohistochemistry. The mRNA and protein levels of AQP3 and stearoyl-CoA desaturase-1 (SCD1) were measured using real-time PCR and western blot, respectively. The cell proliferation was evaluated by CCK8. Result: The total protein concentration of alveolar lavage fluid and the level of inflammatory cytokines such as IL-6 and TNF-a in serum and alveolar lavage fluid were significantly higher in AQP3-/- mice with COPD than that in wide type mice with COPD. Compared with the wide type mice with COPD, the infiltration of inflammatory cells in the lungs of AQP3-/- mice with COPD was significantly increased and the alveolar structure was significantly damaged. The mRNA and protein levels of AQP3 and SCD1 in lung tissue were significantly increased in COPD group in comparison with the control group. In consistent with this, the mRNA and protein levels of AQP3 and SCD1 were increased in HBECs stimulated with cigarette smoke extract. Silencing AQP3 significantly decreased the proliferation ability of HBECs and reduced the expression of SCD1. Furthermore, down-regulation of SCD1 significantly decreased the proliferation ability of HBECs, but did not affect the expression of AQP3. Conclusion: AQP3 has a protective effect on lung inflammation and epithelial injury induced by cigarette smoke. SCD1 plays an important role in this process and is a downstream molecule of AQP3.
Author Block: J. Zhou, G. Zhang, M. Chang, Y. Song, Q. Hong, C. Bai; Department of Pulmonary Medicine, Fudan University, Shanghai, China.
Introduction: Airway epithelial cells are massively damaged in patients with chronic obstructive pulmonary disease (COPD). Aquaporin-3 (AQP3) is highly expressed in the airway epithelial cells in lung. In this study, we investigated the role of AQP3 in COPD airway epithelial cells. Method: The wild-type and AQP3-knockout (AQP3-/-) mice were treated with cigarette smoke and lipopolysaccharides to establish a mouse model of COPD. Human bronchial epithelial cells (HBECs) were stimulated with cigarette smoke extract. Alveolar structure and inflammatory cell infiltration were examined by hematoxylin and eosin staining. The levels of IL-6 and TNF-a in serum and alveolar lavage fluid were evaluated by ELISA. The expression of AQP3 in the lung tissue were detected by immunohistochemistry. The mRNA and protein levels of AQP3 and stearoyl-CoA desaturase-1 (SCD1) were measured using real-time PCR and western blot, respectively. The cell proliferation was evaluated by CCK8. Result: The total protein concentration of alveolar lavage fluid and the level of inflammatory cytokines such as IL-6 and TNF-a in serum and alveolar lavage fluid were significantly higher in AQP3-/- mice with COPD than that in wide type mice with COPD. Compared with the wide type mice with COPD, the infiltration of inflammatory cells in the lungs of AQP3-/- mice with COPD was significantly increased and the alveolar structure was significantly damaged. The mRNA and protein levels of AQP3 and SCD1 in lung tissue were significantly increased in COPD group in comparison with the control group. In consistent with this, the mRNA and protein levels of AQP3 and SCD1 were increased in HBECs stimulated with cigarette smoke extract. Silencing AQP3 significantly decreased the proliferation ability of HBECs and reduced the expression of SCD1. Furthermore, down-regulation of SCD1 significantly decreased the proliferation ability of HBECs, but did not affect the expression of AQP3. Conclusion: AQP3 has a protective effect on lung inflammation and epithelial injury induced by cigarette smoke. SCD1 plays an important role in this process and is a downstream molecule of AQP3.
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