| Autor: |
Salum, Ghada M., Bader El Din, Noha G., Ibrahim, Marwa K., Dawood, Reham M., Farouk, Sally, El Awady, Mostafa K. |
| Předmět: |
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| Zdroj: |
Journal of Interferon & Cytokine Research; Dec2018, Vol. 38 Issue 12, p552-558, 7p |
| Abstrakt: |
Although direct-acting antiviral agents (DAAs) provide hopes for diminution of hepatitis C virus (HCV)-induced liver fibrosis, understanding the molecular mechanisms of crosstalk between signaling pathways in fibrogenesis has remained challenging. In this study, we hypothesize that the mesenchymal–epithelial transition factor (c-MET) and transforming growth factor-β1 (TGF-β1) pathways perform antagonistic functions rather than in concert. One hundred eighteen subjects were selected for this study: 14 controls and 104 chronic HCV patients with different grades of fibrosis (42 F0–F1 and 62 F2–F4). c-MET mRNA was measured by quantitative real-time PCR in peripheral blood mononuclear cells. Since both c-MET and TGF-β1 are secretory proteins, their serum levels were tested by enzyme-linked immunosorbent assay. Although the mRNA expression level of the c-MET gene correlated neither with HCV infection nor with grades of liver fibrosis, serum levels of c-MET and TGF-β1 proteins showed strictly opposite correlation with grades of liver fibrosis. When comparing protein levels in late fibrosis (F2–F4) with levels in early fibrosis (F0–F1), c-MET was significantly decreased (P = 0.001) and TGF-β1 was significantly increased (P = 0.001) at progressive stages of fibrosis. Pearson's correlation coefficient (r = −0.23, P = 0.05) between serum levels of c-MET and TGF-β1 proteins confirms the negative interaction between both pathways. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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