Figure 2.

Ectopic expression of Fendrr aggravates CCl₄-induced liver fibrosis in mice. Mice were injected with oil (oil, n = 5), CCl₄ (CCl4, n = 10), CCl₄ in combination with injection of control lentivirus (CCl4+lv-Ctrl, n = 10) and CCl₄ in combination with injection of lentivirus capable of expressing Fendrr (CCl4+lv-Fendrr, n = 10). The lentivirus was injected once at 2 days before the first CCl₄ injection. A, liver fibrosis was evaluated by H&E staining, sirius red staining as well as collagen I immunohistochemical staining and α-SMA immunofluorescence staining. The scale bar represents 100 μm. B, quantification of the sirius red positive area. C, quantitative evaluation of hepatic hydroxyproline. The hydroxyproline contents are expressed as μg/mg wet liver weight. D, Fendrr expression was examined by qRT-PCR. E, quantification of Col I staining area. F, quantification of α-SMA staining area. G, hepatic Tgfb1, Pdgfa, Col1a1, and Timp1 mRNA expression were examined by qRT-PCR. The results are shown as fold change compared with oil group. H, assessment of serum ALT levels. Data are the mean ± SD of at least three independent experiments. ∗∗p < 0.01, ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001. α-SMA, smooth muscle α-actin; ALT, alanine aminotransferase; Col I, collagen I; qRT-PCR, quantitative real-time PCR; TIMP, tissue inhibitors of metalloproteinase.