Fig. 2: Overexpression of Gfat1 induces hypertrophic growth in cardiomyocytes.
From: Chronic activation of hexosamine biosynthesis in the heart triggers pathological cardiac remodeling

a NRVMs were infected with adenovirus expressing either control GFP (Ad-GFP) or Gfat1 (Ad-Gfat1). Gfat1 protein level was examined by immunoblotting and quantified. GAPDH was used as a loading control. N = 5 for Ad-GFP; n = 6 for Ad-Gfat1. b Representative images of NRVMs stained for α-actinin (red) and the nucleus (DAPI, blue) are shown. Scale: 20 μm. Bar graph depicts relative fold changes in cardiomyocyte surface area normalized to the cells infected by Ad-GFP. N = 91 cells for Ad-GFP; n = 86 cells for Ad-Gfat1. At least three independent experiments were conducted with two to three samples/group/experiment. c Radioactive leucine was included in culture media after Gfat1 overexpression. Leucine incorporation was quantified as indication of protein synthesis. N = 5 for Ad-GFP; n = 6 for Ad-Gfat1. d Overexpression of Gfat1 in NRVMs led to upregulation of hypertrophic marker genes (Anf, Rcan1.4) at the protein levels. N = 5 for Anf; n = 4 for Rcan1. e The hypertrophic marker gene expression was augmented by Gfat1 overexpression at the mRNA levels, as examined by real-time PCR. N = 8 for Anf; n = 3 for Rcan1. Data are shown as mean ± SEM. Student’s t test (two-tailed) was conducted to calculate significance. ***p < 0.001. Source data are provided as a Source Data file.