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. Author manuscript; available in PMC: 2016 Jul 1.
Published in final edited form as: Prog Pediatr Cardiol. 2015 Jan 31;39(1):13–19. doi: 10.1016/j.ppedcard.2015.01.002

Figure 2. Rapamycin normalizes hypertrophic cardiomyopathy in Noonan syndrome with multiple lentigines mice.

Figure 2

(A) Hematoxylin & eosin-stained longitudinal sections of hearts from wild-type (WT) and Noonan syndrome with multiple lentigines (LS/+) mice. Note normalization of hypertrophy in LS/+ hearts after rapamycin treatment (original magnification, ×100). (B) Reticulin stain of paraffin-embedded heart sections from 16-week-old WT and LS/+ mice (original magnification, ×400). (C) Quantification of average area (in μm2) of cardiomyocytes (200–500 cells counted/group) from WT or LS/+ cardiomyocytes isolated from mice that were either vehicle- or rapamycin-treated (2 mg/kg body weight) daily by i.p. injection for 4 weeks, then weekly for 4 weeks. Results are shown as the mean ± standard error of the mean. *P < 0.05, †P < 0.05. (D) Heart weight to body weight ratios of WT and LS/+ mice with vehicle- or rapamycin-treatment, as indicated. *P < 0.05, †P < 0.001. Reprinted with permission from the Journal for Clinical Investigation [35].