Figure 12.

FAPi-treated LX2 HSC modulate macrophage activation and polarization in vitro. (A), Expression of acta2, col1a1, col3a1, timp1, loxl1, tgfb1, and ccl2 in LX2 HSC treated with FAPi. (B–C), Immunofluorescent staining for Ki67 and DAPI in LX2 cells treated with rhFAP and FAPi. (D), Scheme of the experimental design of LX2 CM being added to THP1 cell-derived macrophages. (E–J), Expression of inos, tgfb1, il10, mmp1, mmp9, and mmp14 in PMA-treated (macrophage) THP1 cells after addition of culture medium from LX2 HSC pretreated with and without FAPi. (K), Working model of FAP and FAPi action during liver fibrogenesis. FAP upregulates HSC fibrogenic activation and proliferation and promotes macrophage profibrogenic activation/polarization directly as well as indirectly by production of factors that further promote HSC activation or induce monocyte recruitment (eg, tgfb1 and ccl2, respectively). Data in (A, C, E–J) are means ± standard error of the means (SEMs). Statistical analysis was performed as detailed in Figure 1.