{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,28]],"date-time":"2026-08-28T04:06:19Z","timestamp":1787889979614,"version":"build-2784847793"},"reference-count":21,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2018,2,2]],"date-time":"2018-02-02T00:00:00Z","timestamp":1517529600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81370541"],"award-info":[{"award-number":["81370541"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["81501794"],"award-info":[{"award-number":["81501794"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Medical Virology"],"published-print":{"date-parts":[[2018,5]]},"abstract":"<jats:sec><jats:label\/><jats:p>Hepatic fibrosis is a frequent feature of chronic hepatitis C virus (HCV) infection. Some evidence has suggested the potential role of silent information regulator 1 (SIRT1) in organ fibrosis. The aim of this study was to investigate the effect of HCV core protein on expression of SIRT1 of liver sinusoidal endothelial cell (LSEC) and function of LSEC. LSECs were co\u2010cultured with HepG2 cells or HepG2 cells expressing HCV core protein and LSECs cultured alone were used as controls. After co\u2010culture, the activity and expression levels of mRNA and protein of SIRT1 in LSEC were detected by a SIRT1 fluorometric assay kit, real time\u2010PCR (RT\u2010PCR), Western blot, respectively. The levels of adiponectin receptor 2 (AdipoR2), endothelial nitric oxide synthase (eNOS) and vascular endothelial growth factor (VEGF) were measured by Western blot. Cluster of differentiation 31 (CD31), CD14, and von Willebrand factor (vWf) of LSECs was performed by flow cytometry. The level of reactive oxygen species (ROS) was assayed. Malondialdehyde (MDA), superoxide dismutase (SOD), adiponectin, nitric oxide (NO), and endothelin\u20101 (ET\u20101) levels in the co\u2010culture supernatant were measured. The co\u2010culture supernatant was then used to cultivate LX\u20102 cells. The levels of \u03b1\u2010smooth muscle actin (ASMA) and transforming growth factor\u2010\u03b21 (TGF\u2010\u03b21) protein in LX\u20102 cells were measured by Western blot. Compared with LSEC co\u2010cultured with HepG2 cells group, in LSEC co\u2010cultured with HepG2\u2010core cells group, the activity and expression level of mRNA and protein of SIRT1 reduced; the level of adiponectin reduced and the expression level of AdipoR2 protein decreased; ROS levels increased; the expression level of eNOS, VEGF protein decreased; and the expression level of CD14 decreased; the expression level of vWf and CD31 increased; NO and SOD levels decreased; whereas ET\u20101 and MDA levels increased; the levels of ASMA and TGF\u2010\u03b21 protein in LX\u20102 cells increased. SIRT1 activator improved the above\u2010mentioned changes. HCV core protein may down\u2010regulate the activity and the expression of SIRT1 of LSEC, then decreasing synthesis of adiponectin and the expression of AdipoR2, thus inducing contraction of LSEC and hepatic sinusoidal capillarization and increasing oxidative stress, ultimately cause hepatic stellate cell (HSC) activation. Treatment with SIRT1 activator restored the function of LSEC and inhibited the activation of HSC.<\/jats:p><\/jats:sec>","DOI":"10.1002\/jmv.25034","type":"journal-article","created":{"date-parts":[[2018,1,19]],"date-time":"2018-01-19T13:52:34Z","timestamp":1516369954000},"page":"926-935","source":"Crossref","is-referenced-by-count":28,"title":["Hepatitis C virus core protein induces dysfunction of liver sinusoidal endothelial cell by down\u2010regulation of silent information regulator 1"],"prefix":"10.1002","volume":"90","author":[{"given":"Li\u2010Jie","family":"Sun","sequence":"first","affiliation":[{"name":"Department of Infectious Diseases Second Affiliated Hospital Harbin Medical University Harbin China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3441-9921","authenticated-orcid":false,"given":"Jian\u2010Wu","family":"Yu","sequence":"additional","affiliation":[{"name":"Department of Infectious Diseases Second Affiliated Hospital 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