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. 2014 Apr 25;3(2):e000434. doi: 10.1161/JAHA.113.000434

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© 2014 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.

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Figure 5. — Carbonic anhydrase (CA)‐II exacerbates cardiomyocyte hypertrophy and death in vitro. A, CA‐II overexpression in neonatal and adult cardiomyocytes (nCMs and arCMs, respectively); *P<0.001 vs control empty plasmid (CON). B, Effects of normal/low glucose (CON), high glucose (HG), CA‐II overexpression, CA‐II inhibition by ETZ, and specific NHE‐1 inhibitor (NHE‐1‐i) on nCM cell size; *P<0.004 vs CON, ETZ, HG+ETZ, NHE‐1‐i and CA‐II+NHE‐1‐i. When not specified, drug treated cells were grown in normal/low glucose. C, Effects of normal/low glucose (CON), high glucose, CA‐II overexpression, CA‐II inhibition by ETZ, and specific NHE‐1 inhibitor (NHE‐1‐i) on nCM hypertrophic growth assessed by ^[3H]leucine incorporation; *P<0.001 vs CON, ETZ, HG+ETZ, NHE‐1‐I, and CA‐II+NHE‐1i. D, Effects of normal/low glucose (CON), high glucose, CA‐II overexpression, CA‐II inhibition by ETZ, and specific NHE‐1 inhibitor (NHE‐1‐i) on ANF, BNP and β‐MHC mRNA levels in nCMs; *P<0.001 vs CON, ETZ, HG+ETZ, NHE‐1‐i and CA‐II+NHE‐1i. E, Effects of normal/low glucose (CON), high glucose, CA‐II overexpression, CA‐II inhibition by ETZ, and specific NHE‐1 inhibitor (NHE‐1‐i) on arCM apoptosis; *P<0.001 vs CON, ETZ, HG+ETZ, NHE‐1‐i and CA‐II+NHE‐1i. F, Effects of scrambled control shRNA (CTRL^shRNA) and specific CA‐II shRNA (CA‐II^shRNA) on glucose‐induced NHE‐1 phosphorylation. All quantitative data are from 4 independent experiments. Quantitative data are expressed as mean±SE. EZT indicates 6‐ethoxyzolamide; NHE‐1, sodium‐hydrogen exchanger‐1.