Fig. 3: Gfat1 is required for hypertrophic growth in cardiomyocytes.
From: Chronic activation of hexosamine biosynthesis in the heart triggers pathological cardiac remodeling
a NRVMs were first transfected with either control (ctrl si) or Gfat1 (Gfat1 si) siRNA. PE was then used to trigger cardiomyocyte hypertrophic growth. The cells were harvested for immunofluorescence staining with α-actinin antibody (red) and DAPI (blue). Scale: 20 μm. Quantification showed a significant decrease of cardiomyocyte surface area by Gfat1 silencing. N = 160 cells for ctrl si/veh; n = 102 cells for ctrl si/PE; n = 108 cells for Gfat1 si/veh; n = 140 cells for Gfat1 si/PE. At least three independent experiments were conducted with two to three samples/group/experiment. b Leucine incorporation assay showed Gfat1 knockdown led to strong suppression of cell growth compared with control siRNA. N = 4 for ctrl si/PE group; n = 6 for all other groups. c Representative immunoblots of Gfat1, Rcan1.1, Rcan1.4, and Anf after PE treatment are shown. Quantification is at the right. N = 3–8. d Gfat1 silencing in NRVMs inhibited hypertrophic marker expression at the mRNA levels, as examined by real-time PCR analysis. N = 3–6. Data are shown as mean ± SEM. Significance was calculated by two-way ANOVA, followed by Tukey’s test. ***p < 0.001. Source data are provided as a Source Data file.
