Integrin-linked Kinase And Epithelial-Mesenchymal Transition In The Pathegenesis Of Pulmonary Fibrosis

Objective: To investigate the dynamic expression of Integrin-linked kinase(ILK) and its relation to the Epithelial-Mesenchymal Transition in bleomycin-induced pulmonary fibrosis in mice.Methods: The model of pulmonary fibrosis of mice was duplicated by intraperitoneal injection of bleomycin. All mice were killed on days 28 and 40 after treatment. Lung tissue was stained with HE and Masson-trichrome method. Lung hydroxyproline (HP) content was evaluated. ILK mRNA were analyzed by RT-PCR. Immunohistochemistry and image analysis were used to detect the expression of ILK, alpha-smooth muscle actin (α-SMA) and E-cadherin.Results: Collagen deposition was evident on days 28, alveolar septum was widen, inflammatory cell infiltrated. Collagen deposition reached peak on days 40 and alveolar structure disordered. Lung hydroxyproline (HP) content was increased gradually. Compared to those in the control group, the protein level of ILK andα-SMA was significantly increased in the model group on 28 days and 40 days(p <0.01), while the protein level of E-cadherin was decreased significantly(P <0.01), and the mRNA level of ILK was also increased significantly(P <0.01).Conclusion :1.The mice model of pulmonary fibrosis was successfully established relatively long term i.p administration of bleomycin, which was simulated to manifestation of interstitial pulmonary fibrosis in human.2. The significantly increased expression of ILK in mice pulmonary tissue suggested that ILK played an important role in the pathogenesis of pulmonary fibrosis.3. The expression of E-cadherin was decreased but the expression ofα-SMA was increased suggesting epithelial-mesenchymal transition in mice pulmonary tissue.4. ILK contributes to the pathogenesis of pulmonary fibrosis, which is characterized by EMT.