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. 2018 Oct 16;115(44):E10417–E10426. doi: 10.1073/pnas.1808968115

Fig. 6.

Fig. 6.

Sav1 deletion promotes liver injury and fibrogenesis, leading to NASH progression in Pten-deficient liver. (A) Serum aminotransferase levels in WT, PtenKO, Sav1KO, and Sav1/Pten double-knockout (DKO) mice at 2 mo of age (n = 3 to 4 for each; †P < 0.05 vs. WT and Sav1KO). (B and C) TUNEL staining of liver tissue (B) and the number of TUNEL-positive cells (C) in WT, PtenKO, Sav1KO, and DKO mice (n = 3 to 4 for each; §P < 0.05 vs. WT and PtenKO). (D and E) Ccl2 (D) and Cd68 (E) mRNA abundance in liver tissue of WT, PtenKO, Sav1KO, and DKO mice (n = 3 for each; *P < 0.05 vs. all, **P < 0.05 vs. PtenKO). (F) F4/80 staining of liver tissue in WT, PtenKO, Sav1KO, and DKO mice. (Scale bar: 200 μm.) (G and H) Acta2 (G) and Ctgf (H) mRNA abundance in liver tissue of WT, PtenKO, Sav1KO, and DKO mice (n = 3 for each; *P < 0.05 vs. all). (I) Picro-Sirius Red staining of liver tissue in WT, PtenKO, Sav1KO, and DKO mice. (Scale bar: 200 μm.) (J and K) Col1a1 (J) and Col1a2 (K) mRNA abundance in liver tissue of WT, PtenKO, Sav1KO, and DKO mice (n = 3 for each; *P < 0.05 vs. all).