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. 2016 Jan 22;7:10477. doi: 10.1038/ncomms10477

Figure 8. Cardiac p38γ/δ control heart growth by modulating mTOR activity.

Figure 8

(a–d) Cardiac-specific expression of active p38γ and p38δ mutant forms in p38γ/δ−/− hearts restores normal heart size. p38γ/δ−/− mice were intravenously injected at 4 weeks of age with AAV-TnT-p38γact and AAV-TnT-p38δact, and hearts were harvested from 9-week-old WT, p38γ/δ−/− and p38γ/δ−/− AAV-TnT-p38γ/δact mice. (a) Immunoblot analysis of heart lysates. (b) Top: representative haematoxylin and eosin (H&E) staining of transverse heart sections. Bottom: representative staining with FITC-WGA (green). (c) Cardiomyocyte cross-sectional area quantified from WGA-stained hearts. (d) Heart-weight-to-tibia-length ratio. (e–g) Rapamycin treatment preserves normal heart size in MCKdelta KO hearts. MCK-Cre (control) and MCKdelta KO (p38δMCK−KO) mice were intraperitoneally injected daily with rapamycin (2 mg kg−1 per day) from 4 to 9 weeks of age. (e) Heart-weight-to-tibia-length ratio. (f) Top: representative H&E stained transverse heart sections from 9-week-old MCK-Cre and MCKdelta KO mice after rapamycin treatment. Bottom: representative FITC-WGA staining (green) in hearts from 9-week-old MCK-Cre and MCKdelta KO mice after rapamycin treatment. (g) Echocardiography analysis of 9-week-old MCK-Cre and MCKdelta KO mice treated with rapamycin or vehicle. IVS;d (interventricular septum in diastole); LVPW;d (left ventricle posterior wall in diastole); LV Mass (left ventricle) and ejection fraction. Data are means±s.e.m. (n=5). *P<0.05; **P<0.01; ***P<0.001 (one-way analysis of variance coupled to Bonferroni post test). NS, not significant.