Fig. 4

PRL-1 regulated calcium channels by EGFR-PI3K-CaM calcium signaling in BDL-injured rat livers. a A schematic diagram showing the effects of PRL-1 via EGFR and downstream factors (e.g., IP3R and CaM). b Dot blots and c their intensities using phosphorylated RTK assays; *p  < 0.05 vs. PD-MSCs, **p  < 0.05 vs. PD-MSCs with recombinant PRL-1 (rePRL-1), #p < 0.05 vs. PD-MSCs with rePRL-1 and pentamidine, $p < 0.05 vs. PD-MSCs with rePRL-1. d Western blotting and e and f the intensities of PI3K-p110α and CaM in BDL-induced rat livers. GAPDH was used as a loading control. g CaM expression and h its positive area in BDL-induced rat livers using IHC. Data from each group are shown as the means ± SD and were assessed using Student’s t test. *p  < 0.05 vs. NTx, #p < 0.05 vs. PD-MSCs. BDL, bile duct ligation; CaM, calmodulin; EGFR, epidermal growth factor receptor; GAPDH, glycraldehyde-3-phosphate dehydrogenase; IP3R, inositol trisphosphate receptor; NTx, nontransplantation; PI3K, phosphatidylinositol-3-kinase; PRL-1, phosphatase of regenerating liver-1; RTK, receptor tyrosine kinase