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Inhibition of vascular adhesion protein-1 modifies hepatic steatosis in vitro and in vivo

World Journal of Hepatology 2020年第11期12卷 931-948页

作者： Emma L Shepherd Sumera Karim Philip N Newsome Patricia F Lalor Centre for Liver and Gastroenterology Research Birmingham National Institute for Health ResearchBirmingham Biomedical Research CentreInstitute of Immunology and ImmunotherapyUniversity of BirminghamBirmingham B152TTWest MidlandsUnited Kingdom Liver Unit Queen Elizabeth HospitalUniversity Hospitals BirminghamBirmingham B152TTWest MidlandsUnited Kingdom

BACKGROUND Non-alcoholic fatty liver disease(NAFLD)is associated with obesity,insulin resistance and dyslipidaemia and currently is estimated to affect up to a third of all individuals in developed *** standard of care for patients varies according to disease stage,but includes lifestyle interventions common insulin sensitizers,antioxidants and lipid ***,to date specific therapies have shown little histological or fibrosis stage improvement in large clinical trials,and there is still no licensed therapy for *** the high prevalence,limited treatment options and significant screening costs for the general population,new treatments are urgently *** To assess the potential for inhibition of the amine oxidase enzyme vascular adhesion protein-1(VAP-1)to modify hepatic lipid accumulation in *** We have used immunochemical and qPCR analysis to document expression of VAP-1 and key functional proteins and transporters across the NAFLD *** then utilised hepatocytes in culture and human precision cut liver slices in concert with selective enzyme activity inhibitors to test the effects of activating the semicarbazide-sensitive amine oxidase activity of VAP-1 on hepatic lipid uptake and triglyceride export.A murine model of NAFLD was also used to determine the consequences of VAP-1 knockout and gene expression arrays were used to quantify the effects of VAP-1 activity on key lipid modifying and proinflammatory gene *** We confirmed that increasing severity of NAFLD and progression to cirrhosis was associated with a significant increase in hepatocellular VAP-1 *** in vitro exposed to recombinant VAP-1 and its substrate methylamine showed increased lipid accumulation as determined by quantification of Oil Red O *** was recapitulated using hydrogen peroxide,and lipid accumulation was accompanied by changes in expression of the lipid transporter molecules FABP3,FATP6,insulin recep

关键词： Non-alcoholic fatty liver disease Hepatocyte Lipid Cell biology vascular adhesion protein-1 Steatosis

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