Fig 1: Effect of FAP inhibition on hepatic inflammation in CCl4-induced fibrosis. (A–D), Livers from non-fibrotic mice and mice with fibrosis progression or regression (n = 5–10/group) treated with FAPi and controls were analyzed for macrophage markers CD68 and YM1 using immunohistochemistry in 10 random high-power fields per liver. (E–F), Representative images and quantification of CD3+ T cells in 10 random fields (×200) from the central right lobe of each liver. (G–J), Hepatic transcript levels of inflammation related genes. Data in (C–D, F, G–J) are means ± standard error of the means (SEMs). Statistical analysis was performed as for Figure 1.
Fig 2: FAP inhibition attenuates parenchymal liver fibrosis. (A–C), Livers of mice (n = 5–10/group) treated with FAPi during fibrosis progression or regression vs fibrotic untreated controls were analyzed by quantitative Sirius red and α-SMA immunohistochemistry, performed in 10 random high-power fields per mouse using ImageJ software. (D), Histological fibrosis score of liver sections. (E–F), Hepatic hydroxyproline concentration. (G), Hepatic transcript of fibrosis related transcripts. Data in (B–G) are means ± standard error of the means (SEMs). Statistical analysis was performed as for Figure 1.
Fig 3: Effect of FAP inhibition on liver/spleen weight and general liver inflammation in Mdr2−/− mice. (A), Scheme of FVB control and Mdr2−/− biliary fibrotic mice (n = 5 and n = 10 mice per group, respectively) treated with FAPi (15 or 50 mg/kg bw) or vehicle for 2 weeks. (B−C), Liver/bw ratio and spleen/bw ratio. (D), Representative images of H&E staining from liver sections. (E−H), Serum ALT, AST, ALP, and creatinine levels. Data in (B−C, E−H) are means ± standard errors of the mean (SEMs). Statistical analysis was performed as for Figure 1.
Fig 4: FAP inhibition attenuates hepatic fibrosis in Mdr2−/− mice. (A–E), Livers of nonfibrotic FBV control and biliary fibrotic Mdr2−/− mice (n = 5–10/group) were treated with FAPi (15 or 50 mg/kg/d) for 2 weeks and compared with respective untreated mice. Sirius red stained area and α-SMA-expressing cells in the parenchymal vs septal areas were assessed by quantitative morphometry in 10 high-power fields. (F–G), Total and relative hepatic hydroxyproline concentration. (H–O), Hepatic transcript levels of fibrosis related genes. Data in (B–O) are presented as means ± standard error of the means (SEMs). Statistical analysis was performed as detailed in Figure 1.
Fig 5: FAP expression in CCl4and Mdr2−/− fibrotic livers with/without FAP inhibition and effect of rhFAP/rmFAP on LX-2 HSCs and murine fibroblasts. (A–B), Transcript levels of fap. (C–D), Effect of treatment with rhFAP on LX2 HSCs activation and collagen gene expression. (E–F), Effect of treatment with rmFAP on NIH/3T3 fibroblast activation and collagen gene expression. Data in (A–F) are means ± standard error of the means (SEMs). Statistical analysis was performed as detailed in Figure 1.
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