Figure 1: Acetate rescues hypoxia-induced reduction of histone acetylation.
From: Acetate functions as an epigenetic metabolite to promote lipid synthesis under hypoxia
(a) 1H-NMR spectra of acetate concentration in fresh medium, medium of cancer cells cultured under normoxia or hypoxia. The results represented mean±s.d. of triplicate experiments. (**P<0.01; *P<0.05; by two-tailed unpaired Student’s t-test). (b) Acetate rescues hypoxia-reduced H3K9, H3K27 and H3K56 acetylation levels. HepG2 cells were treated with or without 2.5 mM acetate under hypoxia (1% O2) for 4 h. The histone acetylation levels were determined by western blot. Total H3 served as a loading control. (c) Cancer cells are more sensitive to acetate under hypoxia. HepG2 cells were treated with indicated concentrations of acetate under normoxia or hypoxia (1% O2) for 4 h. The histone acetylation levels were determined by western blot. Total H3 served as a loading control. (d) Acetate increases H3K9, H3K27 and H3K56 acetylation levels in a time-dependent manner under hypoxia. HepG2 cells were treated with or without 5 mM acetate for 0.5, 1, 2 and 4 h under hypoxia (1% O2), respectively. The global histone acetylation levels were determined by western blot. Total histone H3 served as a loading control. (e) Acetate increases H3K9, H3K27 and H3K56 acetylation levels in a dose-dependent manner under hypoxia. HepG2 cells were treated with the indicated concentrations of acetate for 4 h under hypoxia (1% O2). The histone acetylation levels were determined by western blot. Total H3 served as a loading control.
