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. 2018 May 28;9:558. doi: 10.3389/fphys.2018.00558

FIGURE 1.

FIGURE 1

Akap1 deficiency exacerbates pressure overload-induced cardiac hypertrophy. (A) Representative immunoblot (left) and densitometric analysis (right) of AKAP121 protein levels in hearts from sham (n = 5) and 1 week transverse aortic constriction (TAC 1w; n = 7) operated wt, Akap1+/-, and Akap1-/- mice. GAPDH was used as control of loading sample (p < 0.05 vs. wt sham). (B) Bar graphs showing cumulative data of left ventricular weight (LVW) to body weight (BW) 1 week after sham or TAC procedures in wt, Akap1+/-, and Akap1-/- mice (p < 0.05 vs. sham; §p < 0.05 vs. wt TAC 1w; n = 7 hearts/group). (C) (Left) Representative images of wheat germ agglutinin (WGA) staining of cardiac transversal sections from wt, Akap1+/-, and Akap1-/- mice 1 week after sham or TAC procedure. DAPI was used as nuclei counterstaining. Scale bar: 20 μm. (Right) Bar graphs showing cumulative data of multiple independent experiments analyzing cardiomyocytes cross-sectional area (p < 0.05 vs. sham; §p < 0.05 vs. wt TAC 1w; n = 5 hearts/group). (D) mRNA levels of β-myosin heavy chain (β-MHC) in cardiac samples from wt, Akap1+/-, and Akap1-/- mice 1 week after sham or TAC procedure (p < 0.05 vs. sham; n = 5 hearts/group).