Angiotensin II Mediates Cardiomyocyte Hypertrophy in Atrial Cardiomyopathy via Epigenetic Transcriptional Regulation

Figure 4

Regulation of subcellular localization and phosphorylation of HDAC4 and HDAC5. Atrial cardiomyocytes were stimulated with saline, AngII, AngII + losartan, AngII + the PKD inhibitor CID755673, or AngII + the CaMKII inhibitor KN93 for 48 h. The 5 groups were subjected to immunofluorescence staining with an antibody against HDAC4 (a) or HDAC5 (b). The results of the quantitative analysis of the cytosol/total HDAC4 (a), HDAC5 (b) ratio at baseline and after stimulation are shown. (c) Atrial cardiomyocyte extracts from these groups were subjected to western blotting using anti-P-HDAC4 (S246), P-HDAC5 (259), HDAC4, P-HDAC5 (S498), or HDAC5 antibodies. Data are plotted as fold enrichment over equivalent amounts of β-tubulin and are shown as the . . per group. Statistical significance was determined by one-way ANOVA followed by the Bonferroni posttest. Mock: saline, Ang + PKD:AngII + PKD inhibitor CID755673, and Ang + CaMKII:AngII + CaMKII inhibitor KN93.

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