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

Figure 1 Hepatocellular expression of vascular adhesion protein-1 increases in nonalcoholic steatohepatitis. A: Representative brightfield images of sections from indicated disease types stained with Hematoxylin and Eosin (left panels) and Van Geison’s Stain (right panels). Original magnification 10 ×, images representative of multiple fields of view from n = 3 Livers of each disease type. Scale bar is 100 µmol/L; B Immunohistochemical staining for vascular adhesion protein-1 (VAP-1) in representative acetone fixed frozen sections from normal and nonalcoholic steatohepatitis (NASH) livers. Isotype matched control antibody was negative (not shown). Fields were captured at 10 × original magnification with inset pictures captured at 40 × original magnification; C: Analysis of VAP-1 (AOC3) expression by quantitative qPCR analysis. mRNA expression of AOC3 in whole liver RNA from normal, steatotic, NASH, and alcohol-related cirrhosis (ALD) livers using fluidigm qPCR array^®, run on triplicate arrays. Results are expressed as the mean fold change in gene expression normalized to pooled endogenous controls β-actin and GAPDH relative to normal livers defined as 1 ± SEM with means from five normal l, four steatotic, three NASH, and four ALD livers. ^aP < 0.05 or ^bP < 0.01 using a one way ANOVA with Bonferroni correction. NASH: Nonalcoholic steatohepatitis; ALD: Alcohol-related cirrhosis.