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. 2011 Mar;79(3):381–388. doi: 10.1124/mol.110.067298

Fig. 2.

Fig. 2.

Cardiac myocyte cell death, apoptosis, and hypertrophy. A, phenylephrine-induced cell death. Dead cardiac myocytes were counted and expressed as a percentage of total cardiac myocytes. AC6 and AC6mut reduced PE-associated cardiac myocyte death. Bars in graphs are mean values (***, p < 0.001) derived from assessment of 800 to 1000 cells for each condition; experiments were repeated three times. B, phenylephrine-induced myocyte apoptosis. Top, apoptotic cardiac myocytes were detected using TUNEL staining and expressed as -fold increase over untreated myocytes. Bottom, TUNEL-positive cells. AC6 and AC6mut reduced PE-associated cardiac myocyte apoptosis. Bars in graphs are mean values derived from assessment of 500 to 800 cells for each condition; experiments were repeated three times. The p values are from post hoc Bonferroni t testing after one-way ANOVA (**, p < 0.01). C, phenylephrine-induced hypertrophy. Cardiac myocytes infected with Ad.AC6 or Ad.AC6mut were incubated with phenylephrine (20 μM, 44 h), and cardiac myocytes were imaged and cell area (micrometers squared) measured using MetaMorph, an integrated morphometry analysis program. AC6 and AC6mut inhibited PE-induced cardiac myocyte hypertrophy. The p values indicate comparison with control condition with PE. Bars in graphs are mean values (***, p < 0.001) derived from more than 50 cells per condition; experiments were repeated three times.