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. 2010 Feb 21;285(16):11903–11912. doi: 10.1074/jbc.M109.098004

FIGURE 5.

FIGURE 5.

NFATc3 regulates myocardin expression in the hypertrophic pathway of Iso. A, knockdown of NFATc3 by RNAi-A. Cardiomyocytes were infected with adenoviral NFATc3 RNAi-A or its scramble form (NFATc3-S-RNAi-A). NFATc3 protein levels were analyzed by immunoblot 48 h after infection. B, knockdown of NFATc3 attenuates hypertrophic responses induced by Iso. Cardiomyocytes were infected with adenoviruses as described for A. 24 h after infection cells were exposed to 10 μm Iso. Myocardin protein levels were analyzed by immunoblot. Hypertrophy was assessed by measuring cell surface area and protein/DNA ratio 48 h after treatment. *, p < 0.05 versus Iso alone. C, knockdown of NFATc3 by RNAi-B. Cardiomyocytes were infected with adenoviral NFATc3 RNAi-B or its scramble form (NFATc3-S-RNAi-B). NFATc3 protein levels were analyzed by immunoblot 48 h after infection. D, knockdown of NFATc3 attenuates hypertrophic responses induced by Iso. Cardiomyocytes were infected with adenoviruses as described for C. 24 h after infection cells were exposed to 10 μm Iso. Myocardin protein levels were analyzed by immunoblot. Hypertrophy was assessed by measuring cell surface area 48 h after treatment. *, p < 0.05 versus Iso alone. The data are expressed as the means ± S.E. of three independent experiments.