ObjectiveTo investigate the effects of ezrin on transforming growth factor beta (TGF-β) mediated epithelial mesenchymal transition (EMT). MethodsHuman bronchial epithelial 16HBE cells were stimulated by TGF-β to induce EMT. The mRNA and protein levels were analyzed by RT-PCR and Western blot. Lentivirus (LV)-Ezrin-shRNA was employed to investigate the effects of ezrin deficiency on cell morphology and expressions of EMT associated biomarkers including E-cadherin, vimentin, and alpha smooth muscle actin (α-SMA). The effects of recombinant ezrin protein on 16HBE were also examined. ResultsThe expression of ezrin was down-regulated in 16HBE activated by TGF-β. Due to ezrin depletion, the cell morphology changed from a typical multilateral paving stone-like appearance to a mesenchymal-like fusiform appearance along with the decreased expression of epithelium biomarker E-cadherin and the increased mesenchymal cell markers, vimentin and α-SMA. Recombination protein ezrin increased the expression of E-cadherin whilst reducing vimentin and α-SMA. ConclusionTGF-β promotes EMT of 16HBE cells at least partly via inhibiting the expression of ezrin.
Objective To study the effect of secreted frizzled-related protein 1 (SFRP1) on airway remodeling in chronic obstructive pulmonary disease (COPD). Methods Forty-five patients with stable COPD and 21 healthy controls were collected in Jiangsu Province Hospital from June 2014 to June 2016. The level of SFRP1 in serum was detected by ELISA. The expression of SFRP1, E-cadherin and α-smooth muscle actin (α-SMA) in human bronchial epithelial cells (16HBEs) were detected by Western blot. Results The level of SFRP1 in serum of the COPD patients was significantly higher than that in the healthy controls [(80.65 ± 15.01) pg/ml vs. (23.89 ± 2.59) pg/ml, P<0.05]. There were negative correlations between serum SFRP1 levels and lung function parameters (FEV 1, FEV 1%pred, and FVC) in the COPD patients (correlation coefficient r value were –0.368 9, –0.382 6 and –0.417 3, respectively, all P<0.05). The level of serum SFRP1 in the COPD smokers was significantly higher than that in the COPD non-smokers [(97.74 ± 21.95) pg/mlvs. (52.51 ± 14.87) pg/ml, P<0.05]. The expression of SFRP1 could be up-regulated by cigarette smoke extract in 16HBEs. The expression of E-cadherin of 16HBEs was up-regulated by recombinant SFRP1, but the expression of α-SMA of 16HBEs was down-regulated by recombinant SFRP1. Conclusion SFRP1 may be involved in the pathogenesis of airway remodeling of COPD by regulating the expression of E-cadherin and α-SMA of bronchial epithelial cells.