Figure 4.
Delayed signs of liver injury and fibrosis in Asah1P361R/P361R;MCP-1−/− mice. Light micrographs of liver sections stained for hematoxylin and eosin (H&E), Masson’s trichrome, and immunohistochemistry (IHC) for Mac-2 in 8–9-week-old Asah1+/+;MCP-1+/+ mice (A), 8–9-week-old Asah1+/+;MCP-1−/− mice (B), 8–9-week-old Asah1P361R/P361R;MCP-1+/+ mice (C), 8–9-week-old Asah1P361R/P361R;MCP-1−/− mice (D), and 11–12-week-old Asah1P361R/P361R;MCP-1−/− mice (E). The original magnification of the top panel is 20x where the scale bar represents 100 µm and the original magnification of the bottom panel is 40x where the scale bar represents 50 µm. Liver function metabolites and enzymes were analyzed in serum from 8–9-week-old mice for each genotype, and samples from 11–12-week-old Asah1P361R/P361R;MCP-1−/− mice. Analytes from the biochemistry panel include; Albumin (F), alkaline phosphatase (ALP) (G), alanine aminotransferase (ALT) (H), n = 7–9 mice per group. ELISA for aspartate aminotransferase (AST) (I). All comparisons were made between 8–9-week-old Asah1P361R/P361R;MCP-1+/+, 8–9-week-old Asah1P361R/P361R;MCP-1−/− and 11–12-week-old Asah1P361R/P361R;MCP-1−/− mice. n = 8 mice per group. ns (not significant), *p < 0.05, **p < 0.01,***p < 0.001.