Interferon alpha and ribavirin collaboratively regulate p38 mitogen-activated protein kinase signaling in hepatoma cells
| Autor: | Lan-Juan Zhao, Zhong-Tian Qi, Wen Wang, Sheng-Fei He, Hao Ren |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
MAPK/ERK pathway
Carcinoma Hepatocellular MAP Kinase Signaling System p38 mitogen-activated protein kinases Immunology Cell Alpha interferon Hepacivirus Receptor Interferon alpha-beta Transfection p38 Mitogen-Activated Protein Kinases Biochemistry chemistry.chemical_compound Cell Line Tumor Ribavirin medicine Humans Immunology and Allergy Phosphorylation RNA Small Interfering Protein kinase A Molecular Biology Gene knockdown Liver Neoplasms Interferon-alpha virus diseases Drug Synergism Hematology digestive system diseases medicine.anatomical_structure chemistry Cancer research |
| Zdroj: | Cytokine. 61:801-807 |
| ISSN: | 1043-4666 |
| DOI: | 10.1016/j.cyto.2013.01.007 |
| Popis: | Signaling events triggered by interferon alpha (IFN-α) and ribavirin are involved in anti-hepatitis C virus (HCV) action. The p38 mitogen-activated protein kinase (MAPK) pathway plays an important role in HCV pathogenesis. Effects of IFN-α and ribavirin on p38 MAPK signaling were investigated in human hepatoma cells. Type I IFN receptor 2 (IFNAR2) mediated IFN-α-induced p38 MAPK phosphorylation. Also, p38 MAPK phosphorylation was enhanced by ribavirin. Treatment for 48 h with a combination of IFN-α and ribavirin increased p38 MAPK phosphorylation, whereas the treatment for 72 h reduced p38 MAPK phosphorylation. Cell culture-derived HCV (HCVcc) infection dramatically increased p38 MAPK phosphorylation and such phosphorylation was inhibited by IFN-α or ribavirin. Moreover, siRNA-mediated knockdown of p38 MAPK resulted in enhancement of ribavirin-dependent HCV RNA replication. These results suggest that regulation of p38 MAPK signaling by IFN-α and ribavirin might contribute to anti-HCV action. |
| Databáze: | OpenAIRE |
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