![]() ![]() Lung histology demonstrated fibrosis formation and potential epithelia- mesenchymal transition. Expression of epithelial markers including cytokeratin-8, E-cadherin, and prosurfactant protein B decreased. Impaired lung mechanics after mechanical ventilation was associated with increased lung hydroxyproline content, and increased expression of transforming growth factor-β, β-catenin, and mesenchymal markers (α-smooth muscle actin and vimentin) at both the gene and protein levels. To explore the direct effects of mechanical stress on lung fibrotic formation, human lung epithelial cells (BEAS-2B) were exposed to mechanical stretch for up to 48 hrs. The animals were monitored for up to 15 days after acid aspiration. C57BL/6 mice were randomized into four groups: healthy controls hydrochloric acid aspiration alone vehicle control solution followed 24 hrs later by mechanical ventilation (peak inspiratory pressure 22 cm H(2)O and positive end-expiratory pressure 2 cm H(2)O for 2 hrs) and acid aspiration followed 24 hrs later by mechanical ventilation. The objective of this study was t test the hypothesis that mechanical ventilation plays an important role in the pathogenesis of lung fibrosis. ![]() Stresses induced by mechanical ventilation may explain the development of fibrosis by a number of mechanisms (e.g., damage the alveolar epithelium, biotrauma). ![]() Many mechanically ventilated patients with acute respiratory distress syndrome develop pulmonary fibrosis. Mechanical stress induces lung fibrosis by epithelial-mesenchymal transition.Ĭabrera-BenÃtez, Nuria E Parotto, Matteo Post, Martin Han, Bing Spieth, Peter M Cheng, Wei-Erh Valladares, Francisco Villar, Jesús Liu, Mingayo Sato, Masaaki Zhang, Haibo Slutsky, Arthur S Overall, these observations support the beneficial effect of procaterol on airway remodeling frequently associated with chronic obstructive pulmonary diseases. Forskolin, a cyclic adenosine monophosphate-promoting agent, exhibits similar inhibitory activity of procaterol. In addition, procaterol inhibited the expression of adhesion molecules induced during the interaction between eosinophils and bronchial epithelial cells, suggesting the involvement of adhesion molecules in the process of epithelial-mesenchymal transition. Butoxamine, a specific β 2 -adrenergic antagonist, significantly blocked changes induced by procaterol. Procaterol significantly inhibited co-culture associated morphological changes of bronchial epithelial cells, decreased the expression of vimentin, and increased the expression of E-cadherin compared to control. Epithelial-mesenchymal transition was assessed using a co-culture system of human bronchial epithelial cells and primary human eosinophils or an eosinophilic leukemia cell line. In this study, we evaluated whether procaterol can suppress epithelial-mesenchymal transition of airway epithelial cells induced by eosinophils. Procaterol is a selective and full β 2 adrenergic agonist that is used as a rescue of asthmatic attack inhaler form and orally as a controller. We have already reported that epithelial-mesenchymal transition is involved in airway remodeling induced by eosinophils. Kainuma, Keigo Kobayashi, Tetsu D'Alessandro-Gabazza, Corina N Toda, Masaaki Yasuma, Taro Nishihama, Kota Fujimoto, Hajime Kuwabara, Yu Hosoki, Koa Nagao, Mizuho Fujisawa, Takao Gabazza, Esteban CĮpithelial-mesenchymal transition is currently recognized as an important mechanism for the increased number of myofibroblasts in cancer and fibrotic diseases. Î☢ adrenergic agonist suppresses eosinophil- induced epithelial-to-mesenchymal transition of bronchial epithelial cells. ![]()
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