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. 2016 Nov 18;113(49):E7976–E7985. doi: 10.1073/pnas.1617116113

Fig. 7.

Fig. 7.

Mice with the cardiomyocyte-specific SA mutation show cardiac hypertrophy and impaired ventricular performance. (A and B) Immunoblot (A) and quantitation (B) of phosphorylation of CaV1.2 at Ser1700 (pS1700) in heart lysates from mice 10 d after starting treatment with vehicle (Veh) or tamoxifen (TAM, 30 mg/kg) i.p. once daily for three consecutive days. n = 3 for each genotype. (C–F) Echocardiographic assessment of %FS (C), left ventricle MPI (D), Ea/Aa (E), and LVEDD (F) of αMHC-MerCreMer (Cre);Cav1.2WT/lox (n = 5) and Cre;Cav1.2SA/lox (n = 6) mice 4 wk after tamoxifen treatment. (G) HW/BW of the indicated genotypes 5 wk after treatment with vehicle or tamoxifen (n = 5–10 for each group). (H) H&E staining of histological sections of hearts of Cre;Cav1.2SA/lox mice 5 wk after vehicle or tamoxifen treatment. *P < 0.05, ***P < 0.001.