NS5ATP13 Promotes Liver Fibrogenesis via Activation of Hepatic Stellate Cells

摘要: Liver fibrosis is a reversible wound-healing response to any etiology of chronic hepatic injuries. Activation stellate cells (HSCs) the key event in liver fibrogenesis. Generally, persistent activation and proliferation HSCs results progression, while primary mechanisms resolution are apoptosis reversion quiescent phenotype activated HSCs. NS5ATP13 (HCV NS5A-transactivated protein 13) involved nucleologenesis tumorigenesis, but its role HSC remains unclear. This study found that was upregulated both fibrotic tissues human induced by TGF-β1. Moreover, enhanced extracellular matrix (ECM) production activation, with or without TGF-β1 treatment, likely involving TGF-β1/Smad3 signaling pathway. Additionally, boosted inhibiting cell apoptosis. Furthermore, HCV NS5A promoted profibrogenic effect partly through NF-κB p65 (RelA) upregulation. Meanwhile, required for pro-fibrogenic NF-κB. phosphorylation as well were reduced CX-4945, CK2 specific inhibitor. These findings indicated acts factor, providing potential target antifibrotic therapies. J. Cell. Biochem. 118: 2463-2473, 2017. © 2017 Wiley Periodicals, Inc.