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

上皮-间质转化（EMT）被认为参与器官纤维化。然而，在体内肺纤维化的病理生理学中很少有这一过程的直接证据。因此，我们试图证实这一过程参与肺纤维化的发展。由于上皮和间充质标志物的共表达被认为是EMT的标志物，我们进行了双重免疫组织化学，以评估这些蛋白质在博莱霉素诱导的肺纤维化小鼠肺组织中的共表达，以及特发性肺纤维化和非特异性间质性肺炎患者。在博莱霉素诱导的小鼠肺纤维化中很少发现上皮标志物（包括E-cadherin、CD 44 v10、T1α或水通道蛋白5）和间质标志物α-平滑肌肌动蛋白的双阳性细胞。在特发性肺纤维化和非特异性间质性肺炎的肺组织中未发现E-cadherin、ICAM-1、莱亚、CD 44 v9、SP-A和α-平滑肌肌动蛋白的双阳性细胞。与EMT的发生率极低相反，我们偶尔发现具有I型和II型特征的中间细胞或细支气管上皮细胞。这些结果表明，EMT可能存在于肺纤维化，但在肺纤维化的病理生理学中的作用较小。

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.