Fig. 6From: FOXO3a-dependent PARKIN negatively regulates cardiac hypertrophy by restoring mitophagyFOXO3a protected against cardiomyocyte hypertrophy. A, Immunoblotting results of the protein levels of total FOXO3a and phosphorylated FOXO3a in cardiomyocytes treated with Ang II at the indicated time. n = 3 experiments per group. B − D, Overexpression of FOXO3a inhibited Ang II-induced cardiomyocyte hypertrophy. Cardiomyocytes were exposed to Ang II after infected with FOXO3a adenovirus or β-gal adenovirus. B Sarcomere organization stained with phalloidin-TRITC conjugate; bar = 20 µm. Blue represent nucleus. Red represent F-actin. C Cell surface was calculated. *** p < 0.001. n = 3 experiments per group. D The mRNA levels of ANP and BNP were analyzed by qRT-PCR. The results were normalized to GAPDH. * p < 0.05. ** p < 0.01. n = 3 experiments per group. E − G, Knockdown of FOXO3a induced hypertrophic responses. Cardiomyocytes were infected with FOXO3a siRNA or FOXO3a scramble. E Sarcomere organization stained with phalloidin-TRITC conjugate; bar = 20 µm. Blue represent nucleus. Red represent F-actin. F Cell surface was calculated. * p < 0.05. n = 3 experiments per group. G The mRNA levels of ANP and BNP were analyzed by qRT-PCR. The results were normalized to GAPDH. * p < 0.05. ** p < 0.01. n = 3 experiments per groupBack to article page