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. Author manuscript; available in PMC: 2016 Apr 19.
Published in final edited form as: Sci Signal. 2016 Apr 5;9(422):ra34. doi: 10.1126/scisignal.aad5736

Fig. 2. Inhibition of class I HDACs blunts TAC-induced mTOR activity.

Fig. 2

(A) mRNA expression of the hypertrophy markers ANF, BNP and RCAN1.4 from LV after 3 days of TAC and treatment with apicidin (Api, 2 mg/kg) or vehicle (n=4). Veh, vehicle. (B) Western blot analysis of mTOR activity in the left ventricle after TAC for 3 days with quantification (n=6). (C–G) DKO mice 3 weeks after TAC: (C) mRNA expression of hypertrophy markers ANF, BNP, and βMHC (n=4–5). (D) Hematoxylin and eosin staining of four-chamber heart sections after TAC (n=2). Scale bar: 2 mm. (E) Ventricular percent fractional shortening (FS) of control and DKO mice 3 weeks after TAC (n=8–9). (F) Heart weight (HW)/body weight (BW) ratios of control and DKO mice 3 weeks after TAC (n=8). (G) Western blot of S6 and 4EBP1 phosphorylation with quantification (n=4–5). Values are mean ± SEM, analyzed by one-way ANOVA followed by Tukey's test; * denotes p<0.05 sample compared to control (white bar); # denotes p<0.05 between groups marked; n=mice per genotype and treatment.