Figure 1.

FXIIIA deficiency results in decreased cross-linking activities of clots in the early stages after liver injury. A: Time-course of fibronectin and fibrin deposition in control and FXIIIA-null livers at 6 and 24 hours and day 3 after acute liver injury induced by carbon tetrachloride. Double immunofluorescence staining for fibronectin (FN, in red) and fibrin(ogen) (FG, in green), and the merged images. Scale bar = 50 μm. CV, central vein. B: Quantification of colocalized areas between fibronectin and fibrinogen (yellowish fluorescence in each merged figure shown in A; see Materials and Methods) (n = 5 for each group). *P < 0.05. C and D: Western blot analysis of fibrin (FG) (C) and fibronectin (FN) (D) after one-dimensional SDS-PAGE of DOC-insoluble liver samples under reducing conditions. The detection of both fibronectin and fibrin signals was performed in the same membrane using IRDye 800CW- or IRDye 680-conjugated secondary antibodies and the Odyssey Infrared Imaging System (see Materials and Methods). Arrowheads point to top of gels. The positions of a molecular mass marker (kDa) are indicated. Arrows indicate nonreducible high-molecular-weight complexes. The intensity of nonreducible high-molecular-weight bands was measured by densitometry, and the intensity of the control liver at each time point was set to 1. The relative intensities in mutant liver are: fibrinogen, 0.2 at 6 hours, 0.3 at 12 hours, and 0.8 at 24 hours; fibronectin, 0.4 at 6 hours, 0.4 at 12 hours, and 0.6 at 24 hours.