FIGURE 5.
c-Abl regulates MRTF-A activity in hepatic stellate cells. (A) An Acta2 reporter construct or a Col1a1 reporter construct was transfected into LX-2 cells with or without MRTF-A followed by treatment with a c-Abl inhibitor. Luciferase activities were normalized by both protein concentration and GFP fluorescence. (B) LX-2 cells were treated with PDGF-BB in the presence or absence of a c-Abl inhibitor. ChIP assays were performed with anti-MRTF-A. (C,D) An Acta2 reporter construct or a Col1a1 reporter construct was transfected into LX-2 cells with MRTF-A and/or siRNA targeting c-Abl. Knockdown efficiencies were examined by Western. Luciferase activities were normalized by both protein concentration and GFP fluorescence. (E) LX-2 cells were treated with PDGF in the presence or absence of asciminib. ChIP assays were performed with anti-MRTF-A. (F) Primary murine HSCs were activated spontaneously in vitro for 7 days. A c-Abl inhibitor was added at day 5. ChIP assays were performed with anti-MRTF-A. (G) LX-2 cells were transfected with siRNA targeting c-Abl or SCR followed by treatment with PDGF-BB. ChIP assays were performed with anti-MRTF-A. All experiments were repeated three times and one representative experiment is shown. Error bars represent SD (∗p < 0.05, one-way ANOVA with post hoc Scheffe test).