Figure 4.
Impact of TG2 deficiency on hepatic fibrin(ogen) deposition after APAP challenge. Male wild-type and TG2−/− mice were challenged with 300 mg/kg APAP and plasma and liver samples were collected 24 hours later. (A) Representative photomicrographs of fibrinogen labeling (pink) in necrotic areas of liver sections (top: scale bars, 200 μm; bottom: scale bars, 50 μm; arrowheads denote fiber-like labeling in TG2−/− livers, and arrows denote more intense hepatocellular labeling). The dashed box depicts the approximate location of the higher-magnification image below. (B) Insoluble hepatic Fibβ levels were measured in liver extracts using capillary western blotting. The concentration of plasma prothrombin (C), fibrinogen (% of pooled normal mouse plasma) (D), PAP complexes (E), and FDPs (D-dimer) (F) were determined by ELISA. Results from individual mice are plotted and bars represent mean ± SEM. ∗P < .05.

Impact of TG2 deficiency on hepatic fibrin(ogen) deposition after APAP challenge. Male wild-type and TG2−/− mice were challenged with 300 mg/kg APAP and plasma and liver samples were collected 24 hours later. (A) Representative photomicrographs of fibrinogen labeling (pink) in necrotic areas of liver sections (top: scale bars, 200 μm; bottom: scale bars, 50 μm; arrowheads denote fiber-like labeling in TG2−/− livers, and arrows denote more intense hepatocellular labeling). The dashed box depicts the approximate location of the higher-magnification image below. (B) Insoluble hepatic Fibβ levels were measured in liver extracts using capillary western blotting. The concentration of plasma prothrombin (C), fibrinogen (% of pooled normal mouse plasma) (D), PAP complexes (E), and FDPs (D-dimer) (F) were determined by ELISA. Results from individual mice are plotted and bars represent mean ± SEM. ∗P < .05.

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