Fig. 1
From: Histone lysine dimethyl-demethylase KDM3A controls pathological cardiac hypertrophy and fibrosis
KDM3A promotes cardiomyocyte hypertrophy in vitro. a Venn diagram showing differentially expressed genes that are involved in histone methylation and are either up or downregulated in PDE5-Tg versus control littermates, PED5-Tg treated with sildenafil (Reversal) versus control littermates, and reversal versus PDE5-Tg mice after TAC. b KDM3A mRNA in human patients with hypertrophic cardiomyopathy (HCM) (n = 5) and normal controls. *p < 0.05 (t test). c Immunofluorescence micrographs of NRVMs transduced with adenoviruses expressing either LacZ or Kdm3a. Cells were stained with phalloidin. Scale bar, 100 μm. d Relative cell size from cells in c. n = 3 ± SEM, *p < 0.05 (t test). e Relative fold change of mRNA of gene associated with hypertrophic remodeling in NRVMs transduced with either Ad-LacZ or Ad-Kdm3a (n = 3 ± SEM). mRNAs were normalized against internal Gapdh. *p < 0.05 (t test). f–g NRVMs were transfected with control siRNA or Kdm3a specific siRNA, treated with or without PE. Cells were fixed and stained with phalloidin for measurement of cell size (g) or harvested for measurement of relative mRNA of Kdm3a and fetal gene markers (g). mRNA were normalized against internal GAPDH. n = 3 ± SEM, *p < 0.05 (ANOVA)
