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. 2011 Feb 21;121(3):1009–1025. doi: 10.1172/JCI44929

Figure 9. MEK inhibitor treatment rescues growth defect and cardiac hypertrophy in L613V/+ mice.

Figure 9

Mice were injected i.p. daily with PD0325901 (PD; 5 mg/kg BW) or vehicle, starting at 4 weeks of age and for the succeeding 6 weeks. Body length (A) and BW (B) were measured weekly. Note the rapid normalization of body length, as well as the increase in BW caused by inhibitor treatment. #P < 0.05, ##P < 0.005, ###P < 0.0001, 2-way repeated-measures ANOVA; *P < 0.05, **P < 0.005, ***P < 0.0001, Bonferroni post-test when ANOVA was significant (black symbols, WT PD vs. WT control; red symbols, L613V/+ PD vs. L613V/+ control). (C) Heart weight/BW ratio and (D) LVPWd were restored to within normal limits in inhibitor-treated mice. **P < 0.005, ***P < 0.0001, Bonferroni post-test when ANOVA was significant; #P < 0.05, 1-tailed Student’s t test. (E) LVIDd. **P < 0.005, Bonferroni post-test when ANOVA was significant; #P < 0.05, ##P < 0.005, 1-tailed Student’s t test. n = 14 (WT); 10 (L613V/+); 6 (WT PD); 14 (L613V/+ PD). (F) Cross-sectional area of cardiomyocytes (original magnification, ×400; scale bar, 100 μm), measured in WGA-strained heart sections (n = 2 samples per group, with 200 cells counted per sample using ImageJ). ***P < 0.0001, Bonferroni post-test when ANOVA was significant. See also Supplemental Figure 6.