Investigation and regulation of molecular mechanisms of epithelial mesenchymal transition in pulmonary fibrosis

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Epithelial-mesenchymal transition (EMT) has been considered to be involved in organ fibrogenesis. However, there is few direct evidence of this process in the pathophysiology of pulmonary fibrosis in vivo. Therefore, we tried to verify the involvement of this process in the development of pulmonary fibrosis. Since the co-expressions of epithelial and mesenchymal markers are thought to be a marker of EMT, we performed dual immunohistochemistry to assess the co-expressions of these proteins in lung tissues from bleomycin-induced pulmonary fibrosis in mice, and from patients with idiopathic pulmonary fibrosis and nonspecific interstitial pneumonia. Double positive cells for epithelial markers including E-cadherin, CD44v10,T1α, or aquaporin 5,and a mesenchymal marker α-smooth muscle actin were rarely found in bleomycin-induced pulmonary fibrosis in mice. Double positive cells for E-cadherin, ICAM-1,LEA, CD44v9,or SP-A and a-smooth muscle actin were not found in lung tissues from idiopathic pulmonary fibrosis and nonspecific interstitial pneumonia. In contrast to few incidence of EMT, we occasionally found intermediate cells which have characteristics of type I and type II or bronchiolar epithelial cells. These results suggest that EMT may be present in pulmonary fibrosis, but have minor role in the pathophysiology of pulmonary fibrosis.