Review Article
Hepatocyte Turnover in Chronic HCV-Induced Liver Injury and Cirrhosis
Table 1
Apoptotic and antiapoptotic gene expression in chronic HCV-mediated liver injury and cirrhosis.
| Gene/product | Function in CHC | Role |
| Apoptotic | | | IFN- | Upregulation | Cytokine | IRF-7 | Upregulation | Transcription factor | Cytoplasmic dynein light chain | Upregulation | Motor protein, centrosome assembly | AML1/RUNX1 | Upregulation | Transcription factor | Dr-nm23/NME3 | Upregulation | Inhibition of granulocyte differentiation | Plasminogen activator inhibitor-2 | Upregulation | Fibrinolysis, tissue repair | SARP3 | Upregulation | Cellular growth and differentiation | CTGF | Upregulation | Tissue fibrosis, cell adhesion | CDKN1C | Upregulation | Tumor suppressor | CDC42 | Downregulation | Cell cycle progression | Antiapoptotic | | | Bcl-2 | Upregulation | Cell proliferation, oncogenesis | Bcl-w | Upregulation | Cell proliferation | E2F transcription factor | Upregulation | Cell cycle progression | NF-B | Upregulation | Cell proliferation, regeneration | Tissue metalloproteinase inhibitor | Upregulation | Cell-cell interaction, anti-inflammatory cell response |
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CHC: chronic HCV-induced hepatitis; IFN: interferon; IRF: interferon regulatory factor; AML1: acute myeloid leukemia 1 protein; RUNX1: Runt-related transcription factor 1; NME3: nonmetastatic cells protein 3; SARP3: secreted apoptosis-related protein 3; CTGF: connective tissue growth factor; CDKN1C: cyclin-dependent kinase inhibitor 1C; CDC: cell division cycle 42 GTP-binding protein.
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