Fig. 8
WT BM-reconstituted Par2KO mice exhibited apparent hepatitis, while in Par2KO BM-reconstituted WT mice recovered. A, E, and I Par2KO BM-reconstituted WT mice, 1 day after CCl4 injection: hepatic steatosis is apparent with fat vacuoles (arrows). B, F, and J Par2KO BM-reconstituted WT mice, 7 days after injection: hepatic tissue recovered. C, G, and K WT BM-reconstituted Par2KO mice, 1 day after CCl4 injection: hepatic steatosis is apparent with fat vacuoles (arrows, similarly to Par2KO BM-reconstituted WT group). D, H, and L WT BM-reconstituted Par2KO mice, 7 days after CCl4 injection: necrotic lesions (D, H) and collagen fibers (L in pink) appeared. A–D Macroscopic images. E–H H&E, I–L Sirius red. Scale bar = 50μm. M One day after CCl4 administration, it caused similar liver damage in WT, Par2KO, Par2KO, and BM-reconstituted WT and WT BM-reconstituted Par2KO mice. Liver damage at day 1 appeared as clusters of fat vacuoles (E, I, G, and K and in Fig. 7G, L, I, N), and clusters were measured as the number of vacuoles within an area of 25,000μm2. There is no significant difference between groups in liver damage at day 1, n=3–5. N Seven days after CCl4 treatment, liver damage in Par2KO and WT-reconstituted Par2KO mice was more apparent compared to WT and Par2KO-reconstituted WT mice. Liver damage was measured as the percentage area of necrotized lesions, n=5–7. Statistical significance was measured using Mann-Whitney test. *Indicates p<0.05, **p<0.01, ***p<0.005, error bars = SEM