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. 2018 Jan 22;7(2):e005696. doi: 10.1161/JAHA.117.005696

Figure 2.

Figure 2

Cardiac a disintegrin and metalloprotease‐22 (ADAM22) overexpression attenuates the overload‐induced hypertrophic response. A, Schematic of the CAG promoter‐driven mouse cDNA of the ADAM22 transgenic construct. B, Immunoblot and quantification of ADAM22 expression in the hearts of 4 different transgenic founders: 1, 2, 3, and 4. C through E, Levels of left ventricular end diastolic posterior wall dimension (LVPWd), left ventricular end‐diastolic dimension (LVEDD), and fractional shortening (FS) in the indicated groups (n=7 mice in nontransgenic group, and n=12 mice in transgenic group) that received a sham or transverse aortic constriction (TAC) surgery. F through H, The heart weight (HW)/body weight (BW), HW/tibial length (TL), and lung weight (LW)/BW ratios (n=7 mice in nontransgenic group, and n=12 mice in transgenic group). I, Histological analyses of whole heart stained with hematoxylin and eosin (H&E) in the indicated groups (bar=1 mm). J, Histological analyses of the cardiomyocyte cross‐sectional areas (CSAs) after H&E and wheat germ agglutinin staining (bar=20 μm; n=5 mice in nontransgenic group, and n=6 mice in transgenic group). K, Characterization of cardiac interstitial fibrosis after picrosirius red staining (bar=20 μm; n=5 mice in nontransgenic group, and n=6 mice in transgenic group). L, Quantification of hypertrophic markers in the indicated groups (n=4 samples in nontransgenic group, and n=5 samples in transgenic group). Data are representative images or expressed as the mean±SD of each group from at least 3 independent experiments. Statistical analysis was performed by 1‐way analysis of variance and post hoc tests. ACTA indicates acetyl–Coenzyme A acetyltransferase 1; ANP, atrial natriuretic peptide; BNP, B‐type natriuretic peptide; and MHC, myosin heavy chain. *P<0.05 vs nontransgenic/sham group, #P<0.05 vs ADAM22‐transgenic/sham group.