Figure 3.

SIRT6 blocked cardiomyocyte hypertrophy through its deacetylase activity. (A) Western blotting analysis of SIRT6 protein in primary neonatal rat cardiomyocytes transiently transfected with SIRT6 WT (Sirt6) or mutant plasmid (H133Y). (B) The deacetylase activity of SIRT6 was measured in primary neonatal rat cardiomyocytes transfected with Sirt6 or H133Y. (C and D) Primary neonatal rat cardiomyocytes were tansfected with Vector, Sirt6 or H133Y and then treated with or without AngII (100 nM, for 24 h). Cardiomyocyte hypertrophic responses were demonstrated by changes of cell surface areas (C) and mRNA levels of hypertrophic biomarkers ANF, BNP, and β-MHC (D). Data are presented as means ± SE. *P < 0.05, significantly different from. control group, ^#P < 0.05 significantly different from AngII treatment, n= 5.