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

Figure 1.

Figure 1

Increased liver/body weight ratio and hepatocyte proliferation after PH in PTP1B−/− mice. A: Comparison of liver/body weight ratio in PTP1B+/+ and PTP1B−/− mice. Results are given as the mean ± SEM (n = 9–11). B: The PH was performed in PTP1B+/+ and PTP1B−/− mice, and regenerating livers were removed at the indicated periods. The liver regeneration index (liver/body weight ratio) at the indicated periods after PH was calculated. Results are given as the mean ± SEM (n = 6–7). *P < 0.05; **P < 0.01 for PTP1B−/− versus PTP1B+/+ mice. C: Quantification of BrdU-positive nuclei in regenerating livers from PTP1B+/+ and PTP1B−/− mice at 24 to 96 hours after PH. Values are given as the mean ± SEM (n = 4–6). D: Representative microscopic images of BrdU incorporation at 48 and 96 hours after PH. The BrdU-positive nuclei are indicated by arrows. Original magnification, ×10. E: Total protein (50 μg) was analyzed by Western blot, with the antibodies against PCNA, cyclins D1 and E, and β-actin as a loading control. Representative autoradiograms from three independent experiments with similar results are shown. F: Total RNA was isolated from regenerating livers from each genotype, and RT-PCR was performed as described in the corresponding section of Materials and Methods. The IR-deficient immortalized neonatal hepatocytes reconstituted with IRA were used as the control for the IRA isoform. RT-PCR with mouse β-actin primers was performed as a loading control. A representative experiment is shown. Similar results were obtained in two independent series of each genotype of mice.