國家衛生研究院 NHRI:Item 3990099045/13354
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    题名: Type I interferon signaling accelerates liver regeneration by metabolic modulation in noninfectious Conditions
    作者: Wu, MS;Kuo, YP;Lo, YC;Tsai, DJ;Lai, CY;Chuang, TH;Lin, SY;Tsai, WT;Chung, PJ;Yu, GY
    贡献者: National Institute of Infectious Diseases and Vaccinology;Immunology Research Center;Institute of Biomedical Engineering and Nanomedicine
    摘要: Type I interferon (IFN-I) has a well-known function in controlling viral infections, but its contribution in hepatocyte proliferation and hepatocellular carcinoma (HCC) formation remains unclear. Mice deficient in IFN-α receptor expression in whole mice or only in hepatocytes (Ifnar(-/-) and Ifnar(Δliver)) were used to investigate the role of IFN-I signaling in cell proliferation and cancer formation in the liver. We found that Ifnar(-/-) mice were resistant to chemical-induced HCC formation in the absence of infection. Our results showed that low grade of IFN-I and interferon-stimulated gene were expressed substantially in naïve mouse liver. The low level of IFN-I activation is constantly present in mouse liver after weaning and negatively modulates forkhead box O hepatic expression. The IFN-I signaling can be partially blocked by the clearance of lipopolysaccharide. Mice lacking IFN-I signaling have lower basal proliferation activity and delayed liver regeneration processes after two-thirds partial hepatectomy. The activation of IFN-I signaling on hepatocyte controls glucose homeostasis and lipid metabolism to support proliferation potency and long-term tumorigenesis. Our results reveal a positive role of low-grade IFN-I singling to hepatocyte proliferation and HCC formation by modulating glucose homeostasis and lipid metabolism.
    日期: 2021-06
    關聯: American Journal of Pathology. 2021 Jun;191(6):1036-1048.
    Link to: http://dx.doi.org/10.1016/j.ajpath.2021.03.006
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0002-9440&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000654732200007
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85106470268
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