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. 2013 Jan 15;27(2):169–181. doi: 10.1101/gad.204776.112

Figure 3.

Figure 3.

FGF7-mediated LPC activation is conserved in several liver injuries. (A,B) Liver samples prepared from sham-operated (Sham) or BDL mice were subjected to the following experiments. (A) Confocal immunofluorescent double staining using anti-FGF7 (green) and anti-EpCAM (red) antibodies. Bars, 50 μm. (PV) Portal vein. (B) Quantitative RT–PCR analysis of Fgf7 mRNA. Mean ± SE (n = 3). (**) P < 0.01. (C–G) Liver samples from 8-wk-old liver-specific Tak1-LKO (Alfp-Cre; Tak1flox/flox) or control (Tak1flox/flox) mice were subjected to the following experiments. (C) Representative images for immunofluorescent double staining of CK19 (red) and Thy1 (green). (PV) Portal vein. Bars, 80 μm. (D) Confocal immunofluorescent double staining using anti-FGF7 (green) and anti-EpCAM (red) antibodies. Bars, 50 μm. (PV) Portal vein. (E) Quantitative image analysis of CK19-positive area. Mean ± SD (n = 3). (*) P < 0.05. (F) Quantitative image analysis of Thy1-positive area. Mean ± SD (n = 3). (*) P < 0.05. (G) Quantitative RT–PCR analysis of Fgf7 mRNA. Mean ± SD (n = 3). (**) P < 0.01. (H) Serum FGF7 levels in human samples. enzyme-linked immunosorbent assay (ELISA) for human FGF7 was performed on serum samples harvested from healthy controls (n = 6) and patients with fulminant (n = 6) or acute (n = 43) hepatitis. The data are presented as median (25–75 percentile).