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. Author manuscript; available in PMC: 2017 Oct 10.
Published in final edited form as: Cancer Cell. 2016 Oct 10;30(4):595–609. doi: 10.1016/j.ccell.2016.09.004

Figure 7. p62 deficiency in HSC impairs Vitamin D-mediated repression of fibrosis.

Figure 7

(A) Schematic diagram of CCl4-induced fibrosis model and reversion with calcipotriol (Cal). Eight week-old mice were i.p. injected with CCl4 (0.5 ml/kg) three times per week during 4 weeks. Cal (20 μg/kg) was administered via oral gavage five times during the last week of CCl4 treatment. Mice are sacrificed 3 days after the last injection. (B) Sirius red staining of livers of WT (n=6) and GFAP-p62KO (n=7) mice treated as in (A). Scale bars, 100 μm. (C) Sirius red positive area and Ishak score of WT and GFAP-p62KO livers. (D) Immunoblot analysis of αSMA and Actin in WT and GFAP-p62KO livers. (E and F) qPCR analysis of mRNA of HSC activation markers (E) and VDR targets (F) in livers described in (A). Results are presented as mean ± SEM. *p<0.05, **p<0.01, ***p<0.001.