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Fig. 2 | Stem Cell Research & Therapy

Fig. 2

From: Activation of the EGFR-PI3K-CaM pathway by PRL-1-overexpressing placenta-derived mesenchymal stem cells ameliorates liver cirrhosis via ER stress-dependent calcium

Fig. 2

PD-MSCPRL−1 transplantation regulated calcium channels in a rat model of BDL and hepatocytes. a Western blotting and b-f the intensities of calcium channels (e.g., SERCA2b, IP3R, glucose regulated protein 75; GRP75, voltage-dependent anion channel 1; VDAC1, and mitochondria calcium uniporter; MCU) following PD-MSCPRL−1 transplantation in BDL-induced rat liver protein measured using glycraldehyde-3-phosphate dehydrogenase (GAPDH) as a loading control. g Western blotting and h the intensities of calcium channels (e.g., IP3R, GRP75, VDAC1, MCU, and CaM) in TG (500 nM)-treated WB-F344 cells cocultured with PD-MSCs or PD-MSCsPRL−1 for 24 h. α-Tubulin was used as a loading control. i Representative images and j quantification of SERCA2b (green) and ER Tracker (red) in BDL-injured rat livers at 5 weeks using IF staining. DAPI (blue) was used for counterstaining. 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; GAPDH, glycraldehyde-3-phosphate dehydrogenase; GRP75, glucose regulated protein 75; IP3R, inositol trisphosphate receptor; MCU, mitochondrial calcium uniporter; NTx, nontransplantation; PRL-1, phosphatase of regenerating liver-1; SERCA2b, sarco/endoplasmic reticulum Ca2+ ATPase; VDAC1, voltage-dependent anion channel 1

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