Figure 2.

FVIII deficiency did not prevent the development of hepatic fibrin deposits in Plg^−/−mice. (A) Representative HE-stained sections and immunohistochemical stains for fibrin and CD11b-expressing inflammatory cells in livers from WT, F8^−/−, Plg^−/−, and F8^−/−/Plg^−/− mice. Note the hepatic fibrin deposits (arrows) and CD11b⁺ cells (arrowheads) in Plg^−/− and F8^−/−/Plg^−/− mice. The anti-CD11b control is a liver section stained with an isotype antibody (Ab). The fibrin-positive and -negative controls are liver sections from WT and fibrinogen^−/− mice subjected to CCl₄-induced liver injury. Scale bar, 100 µm. The number of fibrin lesions (B) was counted manually, whereas the percentage of fibrin-stained tissue area (C) and the percentage of CD11b-stained tissue area (D) were quantified by digital image analysis. Results are shown as individual observations and mean ± standard error of the mean (SEM). Data were analyzed by the Kruskal-Wallis with Dunn multiple comparisons test. P < .05 was considered significant; *P < .05, **P < .01. All stained slides were scanned at 20× magnification on the Nanozoomer slide scanner (Hamamatsu Photonics K.K.), and quantified with Visiopharm Integrator System software (VIS version 6.7.0.2590; Visiopharm).