Histopathologic and immunohistochemical process parameters (TGF-B1, FSP1/S100A4, ?-smooth muscle actin, collagen type 1 and e-cadherin) fibrogenesis in chronic liver disease with the evaluation

AIM: Liver fibrosis was developed against any toxic or inflammatory damage to the key role in the cell HSH'lerdir over. In this process, a fibrogenic cytokine, TGF-SS function by means of PHM activists to ensure that the restructuring of collagen type I salgılatarak ECM. In recent years, studies on fibrosis PHM activists not only in the extracellular matrix proteins secreted by cells is thought that the EMT. In our study, leading to activation of TGF-SS PHM activists, and all of these phases, the changing relationship between fibrosis and epithelial mesenchymal transformation aimed to demonstrate the presence of cells showing.MATERIALS AND METHODS: Different department with a diagnosis of chronic viral hepatitis, liver biopsy material, 70 patients and 20 control subjects with fibrosis scores by selecting all of the immunohistochemical markers of TGF-ß1, FSP1/S100A4, ?-smooth muscle actin, collagen type I, and E-cadherin was used.RESULTS: CONCLUSIONS: Increased fibrosis and inflammation, TGF-ß1, FSP1/S100A4, ?-smooth muscle actin and collagen type I expression of E-cadherin + increased. This finding suggests a role of these molecules in the process of fibrogenesis. According to HBV in patients with HCV-related chronic hepatitis, especially TGF-ß1, ?-smooth muscle actin and collagen type I expression of E-cadherin + were positively correlated. FSP1/S100A4 apart from other inflammatory cells, fibroblasts also concluded there is no specific boyadığından. Dual immunohistochemical staining was found in the liver hepatocytes are thought to show the EMT.