Wnt Pathway Stabilizes MeCP2 Protein to Repress PPAR-γ in Activation of Hepatic Stellate Cells - Fig 3

<p>(A) The treatment of culture-activated rat HSC on day 5 with DPI (10μM, 24 hr) reverts activated cells to quiescent cells with increased UV-excited vitamin A fluorescence. (B) The DPI treatment reduces MeCP2 and non-phospho(S30/S37/T41)-β-catenin and upregulates PPAR-γ protein in cultured rat HSC. Densitometric results are shown below. (C) The DPI treatment above upregulates <i>Ppar-γ</i> mRNA while suppressing the activation marker <i>Necdin</i>. <i>Mecp2</i> and <i>Ezh2</i> mRNA are also increased. *p<0.05 compared to CTL (vehicle-treated). (D) The DPI treatment has no effects on miR-132 or miR-212 while upregulating miR-137 which was suggested to target <i>Ezh2</i>. *p<0.05 compared to CTL. (E) The treatment with Wnt3a does not rescue DPI-mediated suppression of MeCP2 protein. Ponceau S staining shown below demonstrates equal protein loading.