Lung Epithelial-Mesenchymal Transition Mechanism On Bronchopulmonary Dysplasia

Objective: To investigate the effect of hyperoxia and TGF-β1onepithelial–mesenchymal transition （EMT）of type Ⅱalveolar epithelialcells （AEC-Ⅱ） of mice.Methods: AEC-Ⅱcells （MLE-12lines） were randomly divided intofollowing groups: air exposure group, hyperoxia exposure group, airexposure combined with TGF-β1treatment group, hyperoxia exposurecombined with TGF-β1treatment group. The morphological changes ofcells in each group were observed at6,12,24,48hours. The protein andmRNA expressions of AECⅡspecific marker-lung surfactant protein B（SP-B）and fibroblastspecificmarker-fibroblastspecificprotein （FSP1）were detected by double-labeled immunofluorescence and real time-PCR at the same time point, respectively.Results: Along with the time of exposure to hyperoxia and TGF-β1,AECⅡcells gradually changed from pebble-like shape to spindle shape, andshowed some fibroblast appearances. Synchronously, the protein expressionof SP-B in AECⅡcells decreased, whereas the expression of FSP1increased.The co-expressed were observed at24hours. Comparing with that of the airexposure group, the mRNA expression of SP-B in the hyperoxia exposuregroup, air exposure combined with TGF-β1treatment group, hyperoxiaexposure combined with TGF-β1treatment group decreaseed significantly,whereas the mRNA expression of FSP1increased significantly at24hoursand48hours.Conclusion: Hyperoxia and TGF-β1can induce EMT of type Ⅱalveolar epithelial cells in a time-dependent manner. Objective: To investigate of the expressions epithelial cells marker(lung surfactant protein B,[SP-B]) and fibroblast-specific marker(fibroblast-specific protein,[FSP1]) in newborn mice to explore the role andpathogensis of Epithelial–Mesenchymal Transition(EMT) onbronchopulmonary dysplasia(BPD)Methods: Postnatal day1mice, which were randomly divided intoBPD group hyperoxia exposed and control group exposed in the airrespectively. lung tissues were removed for hematoxylin and eosin(HE)staining for radical alveolar counts(RAC), Masson staining, Double-labeledimmunofluorescence and Q-PCR in order to estimate at postnatal day3,7,14,21of each group the changes of lung morphology and the expression ofSP-B and FSP1protein in BPD mice. BPD mouse for pulmonary functiontesting, evaluation the changes of its physiological and pathologicalfunctions.Results: contrasted the control group, BPD group showed mouse lungtissue developmental disorders and collagen deposition. SP-BmRNA ofBPD group descreased significantly at21d compared with control group(P＜0.05).while FSP1mRNA increased significantly at21d compared withcontrol group(P＜0.05).SP-B and FSP1protein were co-expressed onpostnatal day of14,21in lung tissue by demonstrate Double-labeledimmunofluorescence, which control group was on corresponding.Pulmonary function testing demonstrate respiratory rate (F) and tidal volume(TV) were significantly lower (P <0.05) contrasted the control group. Conclusion: the fibroblast by Epithelial–Mesenchymal Transitionmechanism is an important source of the BPD of pulmonary fibrosis.