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. 2022 Oct 13;77(4):1228–1240. doi: 10.1002/hep.32746

FIGURE 2.

FIGURE 2

Pacritinib treatment JAK2‐dependently blunts fibrogenesis and proliferation in rodent and immortalized human‐derived HSCs. Isolated wild‐type and SM22Cre+‐Jak2f/f mice HSCs were treated with pacritinib at 1 μm during 24 h to measure Col1a1 and p‐moesin protein levels and Col1a1 gene expression (A) and mRNA expression levels of Jak2, Rock, Acta2, and Tgfb (B). TWNT‐4 and LX‐2 human HSCs were treated with pacritinib at 1 μm for 24 h to measure Col1a1 and p‐moesin protein levels and Col1a1 gene expression (C) and mRNA expression of Tgfb, Pdgfrb, Jak2, Rock, and Acta2 in TWNT‐4 and LX2 and Timp1, Col4a1, Pprg, and Lrat in TWNT‐4 (D). BrdU proliferation assay (E); Pcna mRNA expression (F). Results are expressed as the mean ± standard deviation; # p < 0.1. *p < 0.05, **p < 0.01, and ***p < 0.001. Acta2, alpha‐smooth muscle actin; BrdU, bromodeoxyuridine; Col1a1, type I collagen; Col4a1, collagen‐IV; GAPDH, glyceraldehyde‐3‐phosphate dehydrogenase; HSC, hepatic stellate cell; Jak2, Janus kinase 2; Lrat, lecithin‐retinol acyltransferase; NT, nontreated; Pac, pacritinib; Pdgfrb, platelet‐derived growth factor receptor beta; p‐moesin, phospho‐moesin; Pprg, peroxisome proliferator activated receptor gamma; Rock, RhoA/Rho‐kinase; SM22Cre+‐Jak2f/f, floxed‐Jak2 knockout mice with smooth muscle protein 22 Cre‐promotor; Tgfb, transforming growth factor beta; Timp1, tissue inhibitor of metalloproteinases 1; WT, wild type.