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. 2015 Apr 27;29(8):3436–3445. doi: 10.1096/fj.15-271171

Figure 4.

Figure 4.

Increased PKC-dependent activation of canonical TGF-β1 underlies liver fibrosis in LRP6mut/mut mice. A) Western blot analysis demonstrates greater activities of α-SMA, vimentin, hydroxyproline, and PKC/TGF-β pathway in Lrp6mut/mut liver compared to WT mice. Similar results are shown in HepG2 cells after LRP6 knockdown. The relative intensities by densitometry are shown. B) Higher expression of nuclear p-Smad3 in HepG2 cells after LRP6 knockdown is presented. C) After inhibition of PKC and TGF-β by Go 6983 and SB431542, respectively, the LRP6-knockdown HepG2 cells showed lower expression of α-SMA and vimentin vs. controls. D) Colocalization of albumin and a-SMA in mice liver are shown. The insets show 2-fold magnification and arrows indicate the presence of colocalization. The relative intensities by densitometry are shown. Error bars represent SD. *P < 0.05; **P < 0.01. D) The colocalization of albumin with α-SMA in Lrp6mut/mut liver and its comparison with WT mice are shown.