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. 2011 Apr;178(4):1591–1604. doi: 10.1016/j.ajpath.2010.12.020

Figure 7.

Figure 7

Decreased pro-inflammatory signaling and TGF-β–mediated effects during the late phase of liver regeneration in PTP1B−/− mice. A: Left: Western blot analysis of regenerating livers was performed in PTP1B+/+ and PTP1B−/− mice at the indicated periods with the antibodies against phospho-JNK (pJNK) (Thr183/Tyr185), JNK, phospho-c (pc)–Jun (Ser73), phospho-Akt (pAkt) (Ser473), Akt, phospho-ERK (pERK) (Thr202/Tyr204), and ERK. Representative autoradiograms of three independent series of PH in each genotype are shown. Right: Serum alanine aminotransferase activity at different periods after PH. Results are given as the mean ± SEM (n = 4–8). *P < 0.05 for PTP1B−/− versus PTP1B+/+ mice. B: Representative Western blot analysis of regenerating livers with antibodies against SnoN, phospho-Smad2 (Ser465/467)/Smad3 (Ser423/425) (pSmad2/3), Smad2/3, PAI-1, and β-actin as a loading control. Quantification of SnoN and pSmad2/3 from three independent animals in each period was normalized with β-actin or total Smad2/3, respectively. *P < 0.05; **P < 0.01 for PTP1B−/− versus PTP1B+/+ mice. C: Constitutive expression of SnoN in wild-type (Wt), PTP1B−/− (KO), and PTP1B−/−rec (KOrec) immortalized hepatocytes. GAPDH indicates glyceraldehyde-3-phosphate dehydrogenase. D: mRNA levels of PAI-1 were measured by real-time PCR in immortalized PTP1B+/+ and PTP1B−/− hepatocytes stimulated with TGF-β (5 ng/mL) for several periods. Results are given as the mean ± SEM (n = 6). **P < 0.001 for PTP1B−/− versus PTP1B+/+ cells.